Details of the Researcher

PHOTO

Keiko Ando
Section
Graduate School of Dentistry
Job title
Associate Professor
Degree
  • 学術博士(岡山大学)

  • 理学修士(岡山大学)

e-Rad No.
40221741

Research History 8

  • 2019/04 - Present
    Tohoku University Graduate School of Dentistry

  • 2014/10 - 2019/03
    Saitama University Brain Science Institute

  • 2009/08 - 2014/09
    Saitama University

  • 1996/06 - 2009/07
    Tokyo Women's Medical University

  • 1995/01 - 1996/05
    National Defense Medical College

  • 1992/04 - 1994/12
    RIKEN

  • 1991/04 - 1992/03
    独立行政法人 日本学術振興会 特別研究員(PD)

  • 1990/04 - 1991/03
    独立行政法人 日本学術振興会 特別研究員(DC2)

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Education 3

  • Okayama University

    1988/04 - 1991/03

  • Okayama University

    1986/04 - 1988/03

  • Okayama University Faculty of Science

    1982/04 - 1986/03

Professional Memberships 4

  • 歯科基礎医学会

  • 日本動物学会

  • 日本神経科学学会

  • 日本分子生物学会

Research Interests 4

  • 神経回路機能

  • カルシウムイメージング

  • membrane traffic

  • C. elegans

Research Areas 2

  • Life sciences / Neuroscience - general /

  • Life sciences / Cell biology /

Papers 73

  1. Physical Stimulation Methods Developed for In Vitro Neuronal Differentiation Studies of PC12 Cells: A Comprehensive Review. International-journal Peer-reviewed

    Kanako Tominami, Tada-Aki Kudo, Takuya Noguchi, Yohei Hayashi, You-Ran Luo, Takakuni Tanaka, Ayumu Matsushita, Satoshi Izumi, Hajime Sato, Keiko Gengyo-Ando, Atsushi Matsuzawa, Guang Hong, Junichi Nakai

    International journal of molecular sciences 25 (2) 2024/01/07

    DOI: 10.3390/ijms25020772  

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    PC12 cells, which are derived from rat adrenal pheochromocytoma cells, are widely used for the study of neuronal differentiation. NGF induces neuronal differentiation in PC12 cells by activating intracellular pathways via the TrkA receptor, which results in elongated neurites and neuron-like characteristics. Moreover, the differentiation requires both the ERK1/2 and p38 MAPK pathways. In addition to NGF, BMPs can also induce neuronal differentiation in PC12 cells. BMPs are part of the TGF-β cytokine superfamily and activate signaling pathways such as p38 MAPK and Smad. However, the brief lifespan of NGF and BMPs may limit their effectiveness in living organisms. Although PC12 cells are used to study the effects of various physical stimuli on neuronal differentiation, the development of new methods and an understanding of the molecular mechanisms are ongoing. In this comprehensive review, we discuss the induction of neuronal differentiation in PC12 cells without relying on NGF, which is already established for electrical, electromagnetic, and thermal stimulation but poses a challenge for mechanical, ultrasound, and light stimulation. Furthermore, the mechanisms underlying neuronal differentiation induced by physical stimuli remain largely unknown. Elucidating these mechanisms holds promise for developing new methods for neural regeneration and advancing neuroregenerative medical technologies using neural stem cells.

  2. Functional analysis of epilepsy-linked pathogenic variants of the Munc18-1 gene in the inhibitory nervous system of Caenorhabditis elegans. International-journal Peer-reviewed

    Keiko Gengyo-Ando, Akane Osawa-Noguchi, Hideki Ando, Junichi Nakai

    microPublication biology 2024 2024

    DOI: 10.17912/micropub.biology.001174  

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    Heterozygous de novo mutations in Munc18-1, which is essential for neurotransmitter release, cause early infantile epileptic encephalopathy. Munc18-1-linked epilepsy is currently an untreatable disorder and its precise disease mechanism remains elusive. Here, we investigated how Munc18-1 pathogenic variants affect inhibitory neurons using Caenorhabditis elegans . Expression analysis revealed that three missense mutant proteins form aggregates in the cell body of gamma-aminobutyric-acid (GABA)-ergic motoneurons, resulting in a strong reduction of their expression in axons. Their defects of axonal expression correlated closely with pentylenetetrazol-induced convulsions, suggesting that the degree of instability of each mutant protein account for the severity of the epileptic phenotypes.

  3. Domain 3a mutation of VPS33A suppresses larval arrest phenotype in the loss of VPS45 in Caenorhabditis elegans. International-journal Peer-reviewed

    Keiko Gengyo-Ando, Masahiko Kumagai, Hideki Ando, Junichi Nakai

    microPublication biology 2024 2024

    DOI: 10.17912/micropub.biology.001155  

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    The Sec1/Munc18 (SM) protein VPS45 is a key regulator of SNARE-mediated membrane fusion in endosomal trafficking, but its precise role remains unknown. To understand the function of VPS45 in vivo , we performed a genetic suppressor screen in Caenorhabditis elegans . We found that the temperature-sensitive lethality caused by the loss of VPS-45 can be suppressed by a mutation in another SM protein, VPS33A. The VPS33A M376I mutation is located in domain 3a, which is predicted to be essential for SNARE complex assembly. These results highlight the functional importance of domain 3a in endosomal SM proteins and its role in specific membrane fusion.

  4. A humanized Caenorhabditis elegans model for studying pathogenic mutations in VPS45, a protein essential for membrane trafficking, associated with severe congenital neutropenia. International-journal Peer-reviewed

    Keiko Gengyo-Ando, Minoru Tateyama, Shohei Mitani, Hideki Ando, Junichi Nakai

    microPublication biology 2023

    DOI: 10.17912/micropub.biology.001052  

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    VPS45, one of the essential membrane trafficking factors, has been identified as a cause of severe congenital neutropenia 5 (SCN5), but its pathophysiological role remains unknown. Here, we developed a humanized C. elegans model for three pathogenic VPS45 variants. We found that wild-type human VPS45 functionally complemented the loss of C. elegans VPS-45 , and the pathogenic human VPS45 variants functioned almost normally with respect to larval development and endocytosis in C. elegans . These results suggest that SCN5-associated mutations have little effect on the core function of VPS45, and/or that the degree of VPS45 requirement varies, depending on the cell/tissue.

  5. Role of somite patterning in the formation of Weberian apparatus and pleural rib in zebrafish. International-journal Peer-reviewed

    Kagari Akama, Kanami Ebata, Akiteru Maeno, Tomohito Taminato, Shiori Otosaka, Keiko Gengyo-Ando, Junichi Nakai, Kyo Yamasu, Akinori Kawamura

    Journal of anatomy 236 (4) 622-629 2020/04

    DOI: 10.1111/joa.13135  

    ISSN: 0021-8782

    eISSN: 1469-7580

  6. Confocal and multiphoton calcium imaging of the enteric nervous system in anesthetized mice. International-journal Peer-reviewed

    Yuki Motegi, Masaaki Sato, Kazuhide Horiguchi, Masamichi Ohkura, Keiko Gengyo-Ando, Yuji Ikegaya, Yasuyuki Fusamae, Yoshie Hongo, Minoru Suzuki, Koichi Ogawa, Miyako Takaki, Junichi Nakai

    Neuroscience research 151 53-60 2020/02

    DOI: 10.1016/j.neures.2019.02.004  

    ISSN: 0168-0102

    eISSN: 1872-8111

  7. UDP-N-acetylglucosamine-dolichyl-phosphate N-acetylglucosaminephosphotransferase is indispensable for oogenesis, oocyte-to-embryo transition, and larval development of the nematode Caenorhabditis elegans. International-journal Peer-reviewed

    Nanako Kanaki, Ayako Matsuda, Katsufumi Dejima, Daisuke Murata, Kazuko H Nomura, Takashi Ohkura, Keiko Gengyo-Ando, Sawako Yoshina, Shohei Mitani, Kazuya Nomura

    Glycobiology 29 (2) 163-178 2019/02/01

    DOI: 10.1093/glycob/cwy104  

    ISSN: 0959-6658

    eISSN: 1460-2423

  8. Role of tyramine in calcium dynamics of GABAergic neurons and escape behavior in Caenorhabditis elegans. International-journal Peer-reviewed

    Yuko Kagawa-Nagamura, Keiko Gengyo-Ando, Masamichi Ohkura, Junichi Nakai

    Zoological letters 4 19-19 2018

    DOI: 10.1186/s40851-018-0103-1  

    ISSN: 2056-306X

  9. Fast varifocal two-photon microendoscope for imaging neuronal activity in the deep brain. International-journal Peer-reviewed

    Masaaki Sato, Yuki Motegi, Shogo Yagi, Keiko Gengyo-Ando, Masamichi Ohkura, Junichi Nakai

    Biomedical optics express 8 (9) 4049-4060 2017/09/01

    DOI: 10.1364/BOE.8.004049  

    ISSN: 2156-7085

  10. A new platform for long-term tracking and recording of neural activity and simultaneous optogenetic control in freely behaving Caenorhabditis elegans. International-journal Peer-reviewed

    Keiko Gengyo-Ando, Yuko Kagawa-Nagamura, Masamichi Ohkura, Xianfeng Fei, Min Chen, Koichi Hashimoto, Junichi Nakai

    Journal of neuroscience methods 286 56-68 2017/07/15

    DOI: 10.1016/j.jneumeth.2017.05.017  

    ISSN: 0165-0270

    eISSN: 1872-678X

  11. Calcium dynamics regulating the timing of decision-making in C. elegans. International-journal Peer-reviewed

    Yuki Tanimoto, Akiko Yamazoe-Umemoto, Kosuke Fujita, Yuya Kawazoe, Yosuke Miyanishi, Shuhei J Yamazaki, Xianfeng Fei, Karl Emanuel Busch, Keiko Gengyo-Ando, Junichi Nakai, Yuichi Iino, Yuishi Iwasaki, Koichi Hashimoto, Koutarou D Kimura

    eLife 6 2017/05/23

    DOI: 10.7554/eLife.21629  

    ISSN: 2050-084X

  12. Ultra-deep brain imaging with a novel two-photon varifocal microendoscope Peer-reviewed

    Masaaki Sato, Yuki Motegi, Keiko Gengyo-Ando, Masamichi Ohkura, Junichi Nakai

    JOURNAL OF PHARMACOLOGICAL SCIENCES 133 (3) S135-S135 2017/03

    ISSN: 1347-8613

    eISSN: 1347-8648

  13. Distinct roles of the two VPS33 proteins in the endolysosomal system in Caenorhabditis elegans. International-journal Peer-reviewed

    Keiko Gengyo-Ando, Eriko Kage-Nakadai, Sawako Yoshina, Muneyoshi Otori, Yuko Kagawa-Nagamura, Junichi Nakai, Shohei Mitani

    Traffic (Copenhagen, Denmark) 17 (11) 1197-1213 2016/11

    DOI: 10.1111/tra.12430  

    ISSN: 1398-9219

    eISSN: 1600-0854

  14. Characterization of HAF-4- and HAF-9-localizing organelles as distinct organelles in Caenorhabditis elegans intestinal cells. International-journal Peer-reviewed

    Takahiro Tanji, Kenji Nishikori, Syoko Haga, Yuki Kanno, Yusuke Kobayashi, Mai Takaya, Keiko Gengyo-Ando, Shohei Mitani, Hirohisa Shiraishi, Ayako Ohashi-Kobayashi

    BMC cell biology 17 4-4 2016/01/27

    DOI: 10.1186/s12860-015-0076-2  

    ISSN: 1471-2121

  15. REI-1 Is a Guanine Nucleotide Exchange Factor Regulating RAB-11 Localization and Function in C. elegans Embryos. International-journal Peer-reviewed

    Aisa Sakaguchi, Miyuki Sato, Katsuya Sato, Keiko Gengyo-Ando, Tomohiro Yorimitsu, Junichi Nakai, Taichi Hara, Ken Sato, Ken Sato

    Developmental cell 35 (2) 211-21 2015/10/26

    DOI: 10.1016/j.devcel.2015.09.013  

    ISSN: 1534-5807

    eISSN: 1878-1551

  16. Rational design of a high-affinity, fast, red calcium indicator R-CaMP2 (vol 12, pg 64, 2015) Peer-reviewed

    Masatoshi Inoue, Atsuya Takeuchi, Shin-ichiro Horigane, Masamichi Ohkura, Keiko Gengyo-Ando, Hajime Fujii, Satoshi Kamijo, Sayaka Takemoto-Kimura, Masanobu Kano, Junichi Nakai, Kazuo Kitamura, Haruhiko Bito

    NATURE METHODS 12 (9) 893-893 2015/09

    DOI: 10.1038/nmeth0915-893b  

    ISSN: 1548-7091

    eISSN: 1548-7105

  17. Rational design of a high-affinity, fast, red calcium indicator R-CaMP2. International-journal Peer-reviewed

    Masatoshi Inoue, Atsuya Takeuchi, Shin-ichiro Horigane, Masamichi Ohkura, Keiko Gengyo-Ando, Hajime Fujii, Satoshi Kamijo, Sayaka Takemoto-Kimura, Masanobu Kano, Junichi Nakai, Kazuo Kitamura, Haruhiko Bito

    Nature methods 12 (1) 64-70 2015/01

    DOI: 10.1038/nmeth.3185  

    ISSN: 1548-7091

    eISSN: 1548-7105

  18. Generation and Imaging of Transgenic Mice that Express G-CaMP7 under a Tetracycline Response Element. International-journal Peer-reviewed

    Masaaki Sato, Masako Kawano, Masamichi Ohkura, Keiko Gengyo-Ando, Junichi Nakai, Yasunori Hayashi

    PloS one 10 (5) e0125354 2015

    DOI: 10.1371/journal.pone.0125354  

    ISSN: 1932-6203

  19. Amino- and carboxyl-terminal domains of Filamin-A interact with CRMP1 to mediate Sema3A signalling. International-journal Peer-reviewed

    Fumio Nakamura, Kosuke Kumeta, Tomonobu Hida, Toshinari Isono, Yuichi Nakayama, Emiko Kuramata-Matsuoka, Naoya Yamashita, Yutaka Uchida, Ken-ichi Ogura, Keiko Gengyo-Ando, Shohei Mitani, Toshio Ogino, Yoshio Goshima

    Nature communications 5 5325-5325 2014/10/31

    DOI: 10.1038/ncomms6325  

    ISSN: 2041-1723

  20. Arl8/ARL-8 functions in apoptotic cell removal by mediating phagolysosome formation in Caenorhabditis elegans. International-journal Peer-reviewed

    Ayaka Sasaki, Isei Nakae, Maya Nagasawa, Keisuke Hashimoto, Fumiko Abe, Kota Saito, Masamitsu Fukuyama, Keiko Gengyo-Ando, Shohei Mitani, Toshiaki Katada, Kenji Kontani

    Molecular biology of the cell 24 (10) 1584-92 2013/05

    DOI: 10.1091/mbc.E12-08-0628  

    ISSN: 1059-1524

    eISSN: 1939-4586

  21. Large-Scale Screening for Targeted Knockouts in the Caenorhabditis elegans Genome Peer-reviewed

    Robert Barstead, Gary Moulder, Beth Cobb, Stephen Frazee, Diane Henthorn, Jeff Holmes, Daniela Jerebie, Martin Landsdale, Jamie Osborn, Cherilyn Pritchett, James Robertson, John Rummage, Ed Stokes, Malani Vishwanathan, Shohei Mitani, Keiko Gengyo-Ando, Osamu Funatsu, Sayaka Hori, Rieko Imae, Eriko Kage-Nakadai, Hiroyuki Kobuna, Etsuko Machiyama, Tomoko Motohashi, Muneyoshi Otori, Yuji Suehiro, Sawako Yoshina, Donald Moerman, Mark Edgley, Ryan Adair, B. J. Allan, Vinci Au, Iasha Chaudhry, Rene Cheung, Owen Dadivas, Simon Eng, Lisa Fernando, Angela Fisher, Stephane Flibotte, Erin Gilchrist, Allison Hay, Peter Huang, Rebecca Worsley Hunt, Christine Kwitkowski, Joanne Lau, Norris Lee, Lucy Liu, Adam Lorch, Candy Luck, Jason Maydan, Sheldon McKay, Angela Miller, Greg Mullen, Candice Navaroli, Sarah Neil, Rebecca Hunt-Newbury, Mikhaela Partridge, Jaryn Perkins, Anna Rankin, Greta Raymant, Nadereh Rezania, Alexandra Rogula, Bin Shen, Greg Stegeman, Angela Tardif, Jon Taylor, Mariana Veiga, Tina Wang, Rick Zapf

    G3-GENES GENOMES GENETICS 2 (11) 1415-1425 2012/11

    DOI: 10.1534/g3.112.003830  

    ISSN: 2160-1836

  22. Depletion of mboa-7, an enzyme that incorporates polyunsaturated fatty acids into phosphatidylinositol (PI), impairs PI 3-phosphate signaling in Caenorhabditis elegans. International-journal Peer-reviewed

    Hyeon-Cheol Lee, Takuya Kubo, Nozomu Kono, Eriko Kage-Nakadai, Keiko Gengyo-Ando, Shohei Mitani, Takao Inoue, Hiroyuki Arai

    Genes to cells : devoted to molecular & cellular mechanisms 17 (9) 748-57 2012/09

    DOI: 10.1111/j.1365-2443.2012.01624.x  

    ISSN: 1356-9597

    eISSN: 1365-2443

  23. Neuronally expressed Ras-family GTPase Di-Ras modulates synaptic activity in Caenorhabditis elegans. International-journal Peer-reviewed

    Minoru Tada, Keiko Gengyo-Ando, Tetsuo Kobayashi, Masamitsu Fukuyama, Shohei Mitani, Kenji Kontani, Toshiaki Katada

    Genes to cells : devoted to molecular & cellular mechanisms 17 (9) 778-89 2012/09

    DOI: 10.1111/j.1365-2443.2012.01627.x  

    ISSN: 1356-9597

    eISSN: 1365-2443

  24. Physiological function, expression pattern, and transcriptional regulation of a Caenorhabditis elegans insulin-like peptide, INS-18. International-journal Peer-reviewed

    Yohei Matsunaga, Keiko Gengyo-Ando, Shohei Mitani, Takashi Iwasaki, Tsuyoshi Kawano

    Biochemical and biophysical research communications 423 (3) 478-83 2012/07/06

    DOI: 10.1016/j.bbrc.2012.05.145  

    ISSN: 0006-291X

  25. Identification of a novel ADAMTS9/GON-1 function for protein transport from the ER to the Golgi. International-journal Peer-reviewed

    Sawako Yoshina, Kenjiro Sakaki, Aki Yonezumi-Hayashi, Keiko Gengyo-Ando, Hideshi Inoue, Yuichi Iino, Shohei Mitani

    Molecular biology of the cell 23 (9) 1728-41 2012/05

    DOI: 10.1091/mbc.E11-10-0857  

    ISSN: 1059-1524

  26. GPI-anchor synthesis is indispensable for the germline development of the nematode Caenorhabditis elegans. International-journal Peer-reviewed

    Daisuke Murata, Kazuko H Nomura, Katsufumi Dejima, Souhei Mizuguchi, Nana Kawasaki, Yukari Matsuishi-Nakajima, Satsuki Ito, Keiko Gengyo-Ando, Eriko Kage-Nakadai, Shohei Mitani, Kazuya Nomura

    Molecular biology of the cell 23 (6) 982-95 2012/03

    DOI: 10.1091/mbc.E10-10-0855  

    ISSN: 1059-1524

    eISSN: 1939-4586

  27. Single/low-copy integration of transgenes in Caenorhabditis elegans using an ultraviolet trimethylpsoralen method. International-journal Peer-reviewed

    Eriko Kage-Nakadai, Hiroyuki Kobuna, Osamu Funatsu, Muneyoshi Otori, Keiko Gengyo-Ando, Sawako Yoshina, Sayaka Hori, Shohei Mitani

    BMC biotechnology 12 1-1 2012/01/05

    DOI: 10.1186/1472-6750-12-1  

    ISSN: 1472-6750

  28. A Caenorhabditis elegans insulin-like peptide, INS-17: its physiological function and expression pattern. International-journal Peer-reviewed

    Yohei Matsunaga, Kensuke Nakajima, Keiko Gengyo-Ando, Shohei Mitani, Takashi Iwasaki, Tsuyoshi Kawano

    Bioscience, biotechnology, and biochemistry 76 (11) 2168-72 2012

    DOI: 10.1271/bbb.120540  

    ISSN: 0916-8451

    eISSN: 1347-6947

  29. Genetically encoded green fluorescent Ca2+ indicators with improved detectability for neuronal Ca2+ signals. International-journal Peer-reviewed

    Masamichi Ohkura, Takuya Sasaki, Junko Sadakari, Keiko Gengyo-Ando, Yuko Kagawa-Nagamura, Chiaki Kobayashi, Yuji Ikegaya, Junichi Nakai

    PloS one 7 (12) e51286 2012

    DOI: 10.1371/journal.pone.0051286  

    ISSN: 1932-6203

  30. Ceramide glucosyltransferase of the nematode Caenorhabditis elegans is involved in oocyte formation and in early embryonic cell division. International-journal Peer-reviewed

    Kazuko H Nomura, Daisuke Murata, Yasuhiro Hayashi, Katsufumi Dejima, Souhei Mizuguchi, Eriko Kage-Nakadai, Keiko Gengyo-Ando, Shohei Mitani, Yoshio Hirabayashi, Makoto Ito, Kazuya Nomura

    Glycobiology 21 (6) 834-48 2011/06

    DOI: 10.1093/glycob/cwr019  

    ISSN: 0959-6658

  31. Two Golgi-resident 3'-Phosphoadenosine 5'-phosphosulfate transporters play distinct roles in heparan sulfate modifications and embryonic and larval development in Caenorhabditis elegans. International-journal Peer-reviewed

    Katsufumi Dejima, Daisuke Murata, Souhei Mizuguchi, Kazuko H Nomura, Tomomi Izumikawa, Hiroshi Kitagawa, Keiko Gengyo-Ando, Sawako Yoshina, Tomomi Ichimiya, Shoko Nishihara, Shohei Mitani, Kazuya Nomura

    The Journal of biological chemistry 285 (32) 24717-28 2010/08/06

    DOI: 10.1074/jbc.M109.088229  

    ISSN: 0021-9258

    eISSN: 1083-351X

  32. Multivesicular body formation requires OSBP-related proteins and cholesterol. International-journal Peer-reviewed

    Hiroyuki Kobuna, Takao Inoue, Machiko Shibata, Keiko Gengyo-Ando, Akitsugu Yamamoto, Shohei Mitani, Hiroyuki Arai

    PLoS genetics 6 (8) 2010/08/05

    DOI: 10.1371/journal.pgen.1001055  

    ISSN: 1553-7404

  33. The arf-like GTPase Arl8 mediates delivery of endocytosed macromolecules to lysosomes in Caenorhabditis elegans. International-journal Peer-reviewed

    Isei Nakae, Tomoko Fujino, Tetsuo Kobayashi, Ayaka Sasaki, Yorifumi Kikko, Masamitsu Fukuyama, Keiko Gengyo-Ando, Shohei Mitani, Kenji Kontani, Toshiaki Katada

    Molecular biology of the cell 21 (14) 2434-42 2010/07/15

    DOI: 10.1091/mbc.E09-12-1010  

    ISSN: 1059-1524

    eISSN: 1939-4586

  34. An Arf-like small G protein, ARL-8, promotes the axonal transport of presynaptic cargoes by suppressing vesicle aggregation. International-journal Peer-reviewed

    Matthew P Klassen, Ye E Wu, Celine I Maeder, Isei Nakae, Juan G Cueva, Emily K Lehrman, Minoru Tada, Keiko Gengyo-Ando, George J Wang, Miriam Goodman, Shohei Mitani, Kenji Kontani, Toshiaki Katada, Kang Shen

    Neuron 66 (5) 710-23 2010/06/10

    DOI: 10.1016/j.neuron.2010.04.033  

    ISSN: 0896-6273

    eISSN: 1097-4199

  35. Protein phosphatase 2A cooperates with the autophagy-related kinase UNC-51 to regulate axon guidance in Caenorhabditis elegans. International-journal Peer-reviewed

    Ken-ichi Ogura, Takako Okada, Shohei Mitani, Keiko Gengyo-Ando, David L Baillie, Yuji Kohara, Yoshio Goshima

    Development (Cambridge, England) 137 (10) 1657-67 2010/05

    DOI: 10.1242/dev.050708  

    ISSN: 0950-1991

    eISSN: 1477-9129

  36. Two very long chain fatty acid acyl-CoA synthetase genes, acs-20 and acs-22, have roles in the cuticle surface barrier in Caenorhabditis elegans. International-journal Peer-reviewed

    Eriko Kage-Nakadai, Hiroyuki Kobuna, Masako Kimura, Keiko Gengyo-Ando, Takao Inoue, Hiroyuki Arai, Shohei Mitani

    PloS one 5 (1) e8857 2010/01/25

    DOI: 10.1371/journal.pone.0008857  

    ISSN: 1932-6203

  37. FLR-2, the glycoprotein hormone alpha subunit, is involved in the neural control of intestinal functions in Caenorhabditis elegans. International-journal Peer-reviewed

    Akane Oishi, Keiko Gengyo-Ando, Shohei Mitani, Akiko Mohri-Shiomi, Koutarou D Kimura, Takeshi Ishihara, Isao Katsura

    Genes to cells : devoted to molecular & cellular mechanisms 14 (10) 1141-54 2009/10

    DOI: 10.1111/j.1365-2443.2009.01341.x  

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    The intestine plays an essential role in organism-wide regulatory networks in both vertebrates and invertebrates. In Caenorhabditis elegans, class 1 flr genes (flr-1, flr-3 and flr-4) act in the intestine and control growth rates and defecation cycle periods, while class 2 flr genes (flr-2, flr-5, flr-6 and flr-7) are characterized by mutations that suppress the slow growth of class 1 flr mutants. This study revealed that flr-2 gene controls antibacterial defense and intestinal color, confirming that flr-2 regulates intestinal functions. flr-2 encoded the only glycoprotein hormone alpha subunit in C. elegans and was expressed in certain neurons. Furthermore, FLR-2 bound to another secretory protein GHI-1, which belongs to a family of lipid- and lipopolysaccharide-binding proteins. A ghi-1 deletion mutation partially suppressed the short defecation cycle periods of class 1 flr mutants, and this effect was enhanced by flr-2 mutations. Thus, FLR-2 acts as a signaling molecule for the neural control of intestinal functions, which is achieved in a functional network involving class 1 and class 2 flr genes as well as ghi-1. These results are informative to studies of glycoprotein hormone signaling in higher animals.

  38. A Caenorhabditis elegans glycolipid-binding galectin functions in host defense against bacterial infection. International-journal Peer-reviewed

    Hiroko Ideo, Keiko Fukushima, Keiko Gengyo-Ando, Shohei Mitani, Katsufumi Dejima, Kazuya Nomura, Katsuko Yamashita

    The Journal of biological chemistry 284 (39) 26493-501 2009/09/25

    DOI: 10.1074/jbc.M109.038257  

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    Galectins are a family of beta-galactoside-binding proteins that are widely found among animal species and that regulate diverse biological phenomena. To study the biological function of glycolipid-binding galectins, we purified recombinant Caenorhabditis elegans galectins (LEC-1-11) and studied their binding to C. elegans glycolipids. We found that LEC-8 binds to glycolipids in C. elegans through carbohydrate recognition. It has been reported that Cry5B-producing Bacillus thuringiensis strains can infect C. elegans and that the C. elegans Cry5B receptor molecules are glycolipids. We found that Cry5B and LEC-8 bound to C. elegans glycolipid-coated plates in a dose-dependent manner and that Cry5B binding to glycolipids was inhibited by the addition of LEC-8. LEC-8 is usually expressed strongly in the pharyngeal-intestinal valve and intestinal-rectal valve and is expressed weakly in intestine. However, when C. elegans were fed Escherichia coli expressing Cry5B, intestinal LEC-8::EGFP protein levels increased markedly. In contrast, LEC-8::EGFP expression triggered by Cry5B was reduced in toxin-resistant C. elegans mutants, which had mutations in genes involved in biosynthesis of glycolipids. Moreover, the LEC-8-deficient mutant was more susceptible to Cry5B than wild-type worms. These results suggest that the glycolipid-binding lectin LEC-8 contributes to host defense against bacterial infection by competitive binding to target glycolipid molecules.

  39. Functional analysis of GS28, an intra-Golgi SNARE, in Caenorhabditis elegans. International-journal Peer-reviewed

    Masashi Maekawa, Takao Inoue, Hiroyuki Kobuna, Taki Nishimura, Keiko Gengyo-Ando, Shohei Mitani, Hiroyuki Arai

    Genes to cells : devoted to molecular & cellular mechanisms 14 (8) 1003-13 2009/08

    DOI: 10.1111/j.1365-2443.2009.01325.x  

    ISSN: 0037-1017

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    Intra-Golgi retrograde transport is assumed to maintain Golgi function by recycling Golgi-resident proteins to younger cisternae in the progression of entire Golgi stack from cis to trans. GS28 (Golgi SNARE of 28 kDa, also known as GOS28) is a Golgi-localized SNARE protein and has been implicated in intra-Golgi retrograde transport. However, the in vivo functions of GS28, and consequently, the roles of the intra-Golgi retrograde transport in animal development are largely unknown. In this study, we generated deletion mutants of Caenorhabditis elegans GS28 and performed a synthetic lethal RNAi screen using GS28 mutants. We found that another Golgi-localized SNARE, Ykt6, functions cooperatively with GS28 in embryonic development. During post-embryonic development, GS28 mutants exhibited reduced seam cell numbers and a missing ray phenotype under Ykt6 knockdown conditions, suggesting that cell proliferation and/or differentiation of stem cell-like seam cells are impaired in GS28- and Ykt6-depleted worms. We also demonstrated that GS28 and Ykt6 act redundantly for the proper expression of Golgi-resident proteins in adult intestinal cells. This study reveals the in vivo importance of the Golgi-localized SNAREs GS28 and Ykt6.

  40. The ortholog of human solute carrier family 35 member B1 (UDP-galactose transporter-related protein 1) is involved in maintenance of ER homeostasis and essential for larval development in Caenorhabditis elegans. International-journal Peer-reviewed

    Katsufumi Dejima, Daisuke Murata, Souhei Mizuguchi, Kazuko H Nomura, Keiko Gengyo-Ando, Shohei Mitani, Shin Kamiyama, Shoko Nishihara, Kazuya Nomura

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology 23 (7) 2215-25 2009/07

    DOI: 10.1096/fj.08-123737  

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    Although the solute carrier 35B1 (SLC35B1) is evolutionarily conserved, its functions in metazoans remain unknown. To elucidate its function, we examined developmental roles of an SLC35B1 family gene (HUT-1: homolog of UDP-Gal transporter) in Caenorhabditis elegans. We isolated a deletion mutant of the gene and characterized phenotypes of the mutant and hut-1 RNAi-treated worms. GFP-HUT-1 reporter analysis was performed to examine gene expression patterns. We also tested whether several nucleotide sugar transporters can compensate for hut-1 deficiency. The hut-1 deletion mutant and RNAi worms showed larval growth defect and lethality with disrupted intestinal morphology. Inactivation of hut-1 induced chronic endoplasmic reticulum (ER) stress, and hut-1 showed genetic interactions with the atf-6, pek-1, and ire-1 genes involved in unfolded protein response signaling. ER ultrastructure and ER marker distribution in hut-1-deficient animals showed that HUT-1 is required for maintenance of ER structure. Reporter analysis revealed that HUT-1 is an ER protein ubiquitously expressed in tissues, including the intestine. Lethality and the ER stress phenotype of the mutant were rescued with the human hut-1 ortholog UGTrel1. These results indicate important roles for hut-1 in development and maintenance of ER homeostasis in C. elegans.

  41. Normal formation of a subset of intestinal granules in Caenorhabditis elegans requires ATP-binding cassette transporters HAF-4 and HAF-9, which are highly homologous to human lysosomal peptide transporter TAP-like. International-journal Peer-reviewed

    Hiromi Kawai, Takahiro Tanji, Hirohisa Shiraishi, Mitsuo Yamada, Ryoko Iijima, Takao Inoue, Yasuko Kezuka, Kazuaki Ohashi, Yasuo Yoshida, Koujiro Tohyama, Keiko Gengyo-Ando, Shohei Mitani, Hiroyuki Arai, Ayako Ohashi-Kobayashi, Masatomo Maeda

    Molecular biology of the cell 20 (12) 2979-90 2009/06

    DOI: 10.1091/mbc.E08-09-0912  

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    TAP-like (TAPL; ABCB9) is a half-type ATP-binding cassette (ABC) transporter that localizes in lysosome and putatively conveys peptides from cytosol to lysosome. However, the physiological role of this transporter remains to be elucidated. Comparison of genome databases reveals that TAPL is conserved in various species from a simple model organism, Caenorhabditis elegans, to mammals. C. elegans possesses homologous TAPL genes: haf-4 and haf-9. In this study, we examined the tissue-specific expression of these two genes and analyzed the phenotypes of the loss-of-function mutants for haf-4 and haf-9 to elucidate the in vivo function of these genes. Both HAF-4 and HAF-9 tagged with green fluorescent protein (GFP) were mainly localized on the membrane of nonacidic but lysosome-associated membrane protein homologue (LMP-1)-positive intestinal granules from larval to adult stage. The mutants for haf-4 and haf-9 exhibited granular defects in late larval and young adult intestinal cells, associated with decreased brood size, prolonged defecation cycle, and slow growth. The intestinal granular phenotype was rescued by the overexpression of the GFP-tagged wild-type protein, but not by the ATP-unbound form of HAF-4. These results demonstrate that two ABC transporters, HAF-4 and HAF-9, are related to intestinal granular formation and some other physiological aspects.

  42. Member of the membrane-bound O-acyltransferase (MBOAT) family encodes a lysophospholipid acyltransferase with broad substrate specificity. International-journal Peer-reviewed

    Shinji Matsuda, Takao Inoue, Hyeon-Cheol Lee, Nozomu Kono, Fumiharu Tanaka, Keiko Gengyo-Ando, Shohei Mitani, Hiroyuki Arai

    Genes to cells : devoted to molecular & cellular mechanisms 13 (8) 879-88 2008/08

    DOI: 10.1111/j.1365-2443.2008.01212.x  

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    Glycerophospholipids in biological membranes are metabolically active and participate in a series of deacylation-reacylation reactions, which may lead to accumulation of polyunsaturated fatty acids (PUFAs) at the sn-2 position of the glycerol backbone. The reacylation reaction is believed to be catalyzed by acyl-coenzyme A (acyl-CoA):lysophospholipid acyltransferase. Very recently, we have shown that Caenorhabditis elegans mboa-7, which belongs to the membrane-bound O-acyltransferase (MBOAT) family, encodes lysophosphatidylinositol (LPI)-specific acyltransferase (LPIAT). In this study, we found that knockdown of another member of the MBOAT family in C. elegans, named mboa-6, reduced incorporation of exogenous PUFAs into phosphatidylcholine (PC), phosphatidylserine (PS) and phosphatidylethanolamine (PE) in C. elegans. Knockdown of a human mboa-6 homologue, referred to as MBOAT5, also impaired the incorporation of PUFAs into PC, PS and PE in HeLa cells. In in vitro assays, lysoPC (LPC), lysoPS (LPS) and lysoPE (LPE) acyltransferase activities using [(14)C]arachidonoyl-CoA were significantly reduced in the microsomes of MBOAT5 knockdown cells. Conversely, over-expression of MBOAT5 in human embryonic kidney (HEK) 293 cells resulted in great increases in LPC, LPS and LPE acyltransferase activities but not in LPIAT or lysophosphatidic acid (LPA) acyltransferase (LPAAT) activities. These results indicate that human MBOAT5 is a lysophospholipid acyltransferase acting preferentially on LPC, LPS and LPE.

  43. Beta-catenin asymmetry is regulated by PLA1 and retrograde traffic in C. elegans stem cell divisions. International-journal Peer-reviewed

    Takahiro Kanamori, Takao Inoue, Taro Sakamoto, Keiko Gengyo-Ando, Masafumi Tsujimoto, Shohei Mitani, Hitoshi Sawa, Junken Aoki, Hiroyuki Arai

    The EMBO journal 27 (12) 1647-57 2008/06/18

    DOI: 10.1038/emboj.2008.102  

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    Asymmetric division is an important property of stem cells. In Caenorhabditis elegans, the Wnt/beta-catenin asymmetry pathway determines the polarity of most asymmetric divisions. The Wnt signalling components such as beta-catenin localize asymmetrically to the cortex of mother cells to produce two distinct daughter cells. However, the molecular mechanism to polarize them remains to be elucidated. Here, we demonstrate that intracellular phospholipase A(1) (PLA(1)), a poorly characterized lipid-metabolizing enzyme, controls the subcellular localizations of beta-catenin in the terminal asymmetric divisions of epithelial stem cells (seam cells). In mutants of ipla-1, a single C. elegans PLA(1) gene, cortical beta-catenin is delocalized and the asymmetry of cell-fate specification is disrupted in the asymmetric divisions. ipla-1 mutant phenotypes are rescued by expression of ipla-1 in seam cells in a catalytic activity-dependent manner. Furthermore, our genetic screen utilizing ipla-1 mutants reveals that reduction of endosome-to-Golgi retrograde transport in seam cells restores normal subcellular localization of beta-catenin to ipla-1 mutants. We propose that membrane trafficking regulated by ipla-1 provides a mechanism to control the cortical asymmetry of beta-catenin.

  44. Role of C. elegans TAT-1 protein in maintaining plasma membrane phosphatidylserine asymmetry. International-journal Peer-reviewed

    Monica Darland-Ransom, Xiaochen Wang, Chun-Ling Sun, James Mapes, Keiko Gengyo-Ando, Shohei Mitani, Ding Xue

    Science (New York, N.Y.) 320 (5875) 528-31 2008/04/25

    DOI: 10.1126/science.1155847  

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    The asymmetrical distribution of phospholipids on the plasma membrane is critical for maintaining cell integrity and physiology and for regulating intracellular signaling and important cellular events such as clearance of apoptotic cells. How phospholipid asymmetry is established and maintained is not fully understood. We report that the Caenorhabditis elegans P-type adenosine triphosphatase homolog, TAT-1, is critical for maintaining cell surface asymmetry of phosphatidylserine (PS). In animals deficient in tat-1, PS is abnormally exposed on the cell surface, and normally living cells are randomly lost through a mechanism dependent on PSR-1, a PS-recognizing phagocyte receptor, and CED-1, which contributes to recognition and engulfment of apoptotic cells. Thus, tat-1 appears to function in preventing appearance of PS in the outer leaflet of plasma membrane, and ectopic exposure of PS on the cell surface may result in removal of living cells by neighboring phagocytes.

  45. Caenorhabditis elegans mboa-7, a member of the MBOAT family, is required for selective incorporation of polyunsaturated fatty acids into phosphatidylinositol. International-journal Peer-reviewed

    Hyeon-Cheol Lee, Takao Inoue, Rieko Imae, Nozomu Kono, Shinichiro Shirae, Shinji Matsuda, Keiko Gengyo-Ando, Shohei Mitani, Hiroyuki Arai

    Molecular biology of the cell 19 (3) 1174-84 2008/03

    eISSN: 1939-4586

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    Phosphatidylinositol (PI) is a component of membrane phospholipids, and it functions both as a signaling molecule and as a compartment-specific localization signal in the form of polyphosphoinositides. Arachidonic acid (AA) is the predominant fatty acid in the sn-2 position of PI in mammals. LysoPI acyltransferase (LPIAT) is thought to catalyze formation of AA-containing PI; however, the gene that encodes this enzyme has not yet been identified. In this study, we established a screening system to identify genes required for use of exogenous polyunsaturated fatty acids (PUFAs) in Caenorhabditis elegans. In C. elegans, eicosapentaenoic acid (EPA) instead of AA is the predominant fatty acid in PI. We showed that an uncharacterized gene, which we named mboa-7, is required for incorporation of PUFAs into PI. Incorporation of exogenous PUFA into PI of the living worms and LPIAT activity in the microsomes were greatly reduced in mboa-7 mutants. Furthermore, the membrane fractions of transgenic worms expressing recombinant MBOA-7 and its human homologue exhibited remarkably increased LPIAT activity. mboa-7 encodes a member of the membrane-bound O-acyltransferase family, suggesting that mboa-7 is LPIAT. Finally, mboa-7 mutants had significantly lower EPA levels in PI, and they exhibited larval arrest and egg-laying defects.

  46. Control of sex-specific apoptosis in C. elegans by the BarH homeodomain protein CEH-30 and the transcriptional repressor UNC-37/Groucho. International-journal Peer-reviewed

    Erin Peden, Elizabeth Kimberly, Keiko Gengyo-Ando, Shohei Mitani, Ding Xue

    Genes & development 21 (23) 3195-207 2007/12/01

    ISSN: 0890-9369

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    Apoptosis is essential for proper development and tissue homeostasis in metazoans. It plays a critical role in generating sexual dimorphism by eliminating structures that are not needed in a specific sex. The molecular mechanisms that regulate sexually dimorphic apoptosis are poorly understood. Here we report the identification of the ceh-30 gene as a key regulator of sex-specific apoptosis in Caenorhabditis elegans. Loss-of-function mutations in ceh-30 cause the ectopic death of male-specific CEM neurons. ceh-30 encodes a BarH homeodomain protein that acts downstream from the terminal sex determination gene tra-1, but upstream of, or in parallel to, the cell-death-initiating gene egl-1 to protect CEM neurons from undergoing apoptosis in males. The second intron of the ceh-30 gene contains two adjacent cis-elements that are binding sites for TRA-1A and a POU-type homeodomain protein UNC-86 and acts as a sensor to regulate proper specification of the CEM cell fate. Surprisingly, the N terminus of CEH-30 but not its homeodomain is critical for CEH-30's cell death inhibitory activity in CEMs and contains a conserved eh1/FIL domain that is important for the recruitment of the general transcriptional repressor UNC-37/Groucho. Our study suggests that ceh-30 defines a critical checkpoint that integrates the sex determination signal TRA-1 and the cell fate determination and survival signal UNC-86 to control the sex-specific activation of the cell death program in CEMs through the general transcription repressor UNC-37.

  47. The PLEXIN PLX-2 and the ephrin EFN-4 have distinct roles in MAB-20/Semaphorin 2A signaling in Caenorhabditis elegans morphogenesis. International-journal Peer-reviewed

    Fumi Nakao, Martin L Hudson, Motoshi Suzuki, Zachary Peckler, Rie Kurokawa, Zhicen Liu, Keiko Gengyo-Ando, Akira Nukazuka, Takashi Fujii, Fumikazu Suto, Yukimasa Shibata, Go Shioi, Hajime Fujisawa, Shohei Mitani, Andrew D Chisholm, Shin Takagi

    Genetics 176 (3) 1591-607 2007/07

    ISSN: 0016-6731

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    Semaphorins are extracellular proteins that regulate axon guidance and morphogenesis by interacting with a variety of cell surface receptors. Most semaphorins interact with plexin-containing receptor complexes, although some interact with non-plexin receptors. Class 2 semaphorins are secreted molecules that control axon guidance and epidermal morphogenesis in Drosophila and Caenorhabditis elegans. We show that the C. elegans class 2 semaphorin MAB-20 binds the plexin PLX-2. plx-2 mutations enhance the phenotypes of hypomorphic mab-20 alleles but not those of mab-20 null alleles, indicating that plx-2 and mab-20 act in a common pathway. Both mab-20 and plx-2 mutations affect epidermal morphogenesis during embryonic and in postembryonic development. In both contexts, plx-2 null mutant phenotypes are much less severe than mab-20 null phenotypes, indicating that PLX-2 is not essential for MAB-20 signaling. Mutations in the ephrin efn-4 do not synergize with mab-20, indicating that EFN-4 may act in MAB-20 signaling. EFN-4 and PLX-2 are coexpressed in the late embryonic epidermis where they play redundant roles in MAB-20-dependent cell sorting.

  48. C. elegans mitochondrial factor WAH-1 promotes phosphatidylserine externalization in apoptotic cells through phospholipid scramblase SCRM-1. International-journal Peer-reviewed

    Xiaochen Wang, Jin Wang, Keiko Gengyo-Ando, Lichuan Gu, Chun-Ling Sun, Chonglin Yang, Yong Shi, Tetsuo Kobayashi, Yigong Shi, Shohei Mitani, Xiao-Song Xie, Ding Xue

    Nature cell biology 9 (5) 541-9 2007/05

    ISSN: 1465-7392

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    Externalization of phosphatidylserine, which is normally restricted to the inner leaflet of plasma membrane, is a hallmark of mammalian apoptosis. It is not known what activates and mediates the phosphatidylserine externalization process in apoptotic cells. Here, we report the development of an annexin V-based phosphatidylserine labelling method and show that a majority of apoptotic germ cells in Caenorhabditis elegans have surface-exposed phosphatidylserine, indicating that phosphatidylserine externalization is a conserved apoptotic event in worms. Importantly, inactivation of the gene encoding either the C. elegans apoptosis-inducing factor (AIF) homologue (WAH-1), a mitochondrial apoptogenic factor, or the C. elegans phospholipid scramblase 1 (SCRM-1), a plasma membrane protein, reduces phosphatidylserine exposure on the surface of apoptotic germ cells and compromises cell-corpse engulfment. WAH-1 associates with SCRM-1 and activates its phospholipid scrambling activity in vitro. Thus WAH-1, after its release from mitochondria during apoptosis, promotes plasma membrane phosphatidylserine externalization through its downstream effector, SCRM-1.

  49. IFT-81 and IFT-74 are required for intraflagellar transport in C. elegans. International-journal Peer-reviewed

    Tetsuo Kobayashi, Keiko Gengyo-Ando, Takeshi Ishihara, Isao Katsura, Shohei Mitani

    Genes to cells : devoted to molecular & cellular mechanisms 12 (5) 593-602 2007/05

    ISSN: 1356-9597

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    Intraflagellar transport (IFT) is essential machinery for biogenesis and maintenance of cilia in many eukaryotic and prokaryotic cells. A large number of polypeptides are known to be involved in IFT, but the physiological role of each component is not fully elucidated. Here, we identified a C. elegans orthologue of a Chlamydomonas reinhardtii IFT component, IFT-81, and found that its loss-of-function mutants show an unusual behavioral property and small body size. IFT-81 is expressed in sensory neurons, and localized at the base of cilia. The similar phenotypes with ift-81 mutants were also observed in several IFT mutants, suggesting these defects are caused by inability of IFT. We also demonstrated that IFT-81 interacts and co-localizes with IFT-74, which is another putative component of IFT. The ift-74 loss-of-function mutants showed phenocopies with ift-81 mutants, suggesting IFT-81 and IFT-74 play comparable functions. Moreover, ift-81 and ift-74 mutants similarly exhibited weak anomalies in cilia formation and obvious disruptions of transport in mature cilia. Thus, we conclude that IFT-81 and IFT-74 coordinately act in IFT in C. elegans sensory cilia.

  50. Expression of rib-1, a Caenorhabditis elegans homolog of the human tumor suppressor EXT genes, is indispensable for heparan sulfate synthesis and embryonic morphogenesis. International-journal Peer-reviewed

    Hiroshi Kitagawa, Tomomi Izumikawa, Souhei Mizuguchi, Katsufumi Dejima, Kazuko H Nomura, Noriyuki Egusa, Fumiyasu Taniguchi, Jun-ichi Tamura, Keiko Gengyo-Ando, Shohei Mitani, Kazuya Nomura, Kazuyuki Sugahara

    The Journal of biological chemistry 282 (11) 8533-44 2007/03/16

    ISSN: 0021-9258

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    The proteins encoded by all of the five cloned human EXT family genes (EXT1, EXT2, EXTL1, EXTL2, and EXTL3), members of the hereditary multiple exostoses gene family of tumor suppressors, are glycosyltransferases required for the biosynthesis of heparan sulfate. In the Caenorhabditis elegans genome, only two genes, rib-1 and rib-2, homologous to the mammalian EXT genes have been identified. Although rib-2 encodes an N-acetylglucosaminyltransferase involved in initiating the biosynthesis and elongation of heparan sulfate, the involvement of the protein encoded by rib-1 in the biosynthesis of heparan sulfate remains unclear. Here we report that RIB-1 is indispensable for the biosynthesis and for embryonic morphogenesis. Despite little individual glycosyltransferase activity by RIB-1, the polymerization of heparan sulfate chains was demonstrated when RIB-1 was coexpressed with RIB-2 in vitro. In addition, RIB-1 and RIB-2 were demonstrated to interact by pulldown assays. To investigate the functions of RIB-1 in vivo, we depleted the expression of rib-1 by deletion mutagenesis. The null mutant worms showed reduced synthesis of heparan sulfate and embryonic lethality. Notably, the null mutant embryos showed abnormality at the gastrulation cleft formation stage or later and arrested mainly at the 1-fold stage. Nearly 100% of the embryos died before L1 stage, although the differentiation of some of the neurons and muscle cells proceeded normally. Similar phenotypes have been observed in rib-2 null mutant embryos. Thus, RIB-1 in addition to RIB-2 is indispensable for the biosynthesis of heparan sulfate in C. elegans, and the two cooperate to synthesize heparan sulfate in vivo. These findings also show that heparan sulfate is essential for post-gastrulation morphogenic movement of embryonic cells and is indispensable for ensuring the normal spatial organization of differentiated tissues and organs.

  51. ASB-1, a germline-specific isoform of mitochondrial ATP synthase b subunit, is required to maintain the rate of germline development in Caenorhabditis elegans. International-journal Peer-reviewed

    Ichiro Kawasaki, Momoyo Hanazawa, Keiko Gengyo-Ando, Shohei Mitani, Ichiro Maruyama, Yuichi Iino

    Mechanisms of development 124 (3) 237-51 2007/03

    ISSN: 0925-4773

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    The developmental timing of all types of cells must be synchronized and spatially coordinated to achieve the organized development of a multicellular organism. Previously, we found RNAi of asb-1, encoding a germline-specific isoform of mitochondrial ATP synthase b subunit, caused 100% penetrant sterility in Caenorhabditis elegans. ATP synthase is one of the five complexes of the mitochondrial respiratory chain, and defects in some of the components of the chain are known to slow the growth and extend the lifespan of worms. We found that development of asb-1 mutant germ line was not arrested at any stage, but did slow to half the rate of wild type, whereas the rate of somatic development was the same in asb-1 mutants as that of wild type, indicating that asb-1 is required to maintain the rate of germline development but has no effect on somatic development. Among ATP synthase subunit genes, RNAi of asg-1, encoding a germline-specific isoform of the g subunit, also caused asb-1-like sterility, indicating that some other germline-specific components are also required to maintain the rate of germline development. Both asb-1 and asg-1 are located on autosomes while they possess counterparts, asb-2 and asg-2, respectively, on X chromosome, which are both required for somatic development. Chromosomal locations of the genes may be the basis of the segregation of germline/somatic functions of each gene, as were demonstrated for other autosomal/X-linked duplicated gene pairs.

  52. The SM protein VPS-45 is required for RAB-5-dependent endocytic transport in Caenorhabditis elegans. International-journal Peer-reviewed

    Keiko Gengyo-Ando, Hidehito Kuroyanagi, Tetsuo Kobayashi, Motohide Murate, Kazushi Fujimoto, Shigeo Okabe, Shohei Mitani

    EMBO reports 8 (2) 152-7 2007/02

    ISSN: 1469-221X

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    Rab5, a small guanosine triphosphatase, is known to regulate the tethering and docking reaction leading to SNARE (soluble NSF attachment protein receptors)-mediated fusion between endosomes. However, it is uncertain how the signal of the activated Rab5 protein is transduced by its downstream effectors during endosome fusion. Here, we show that the Sec1/Munc18 gene vps-45 is essential for not only viability and development but also receptor-mediated and fluid-phase endocytosis pathways in Caenorhabditis elegans. We found that VPS-45 interacts with a Rab5 effector, Rabenosyn-5 (RABS-5), and the mutants of both vps-45 and rabs-5 show similar endocytic phenotypes. In the macrophage-like cells of vps-45 and rabs-5 mutants, aberrantly small endosomes were accumulated, and the endosome fusion stimulated by the mutant RAB-5 (Q78L) is suppressed by these mutations. Our results indicate that VPS-45 is a key molecule that functions downstream from RAB-5, cooperating with RABS-5, to regulate the dynamics of the endocytic system in multicellular organisms.

  53. Disruption of ins-11, a Caenorhabditis elegans insulin-like gene, and phenotypic analyses of the gene-disrupted animal. International-journal Peer-reviewed

    Tsuyoshi Kawano, Ryosuke Nagatomo, Yasuo Kimura, Keiko Gengyo-Ando, Shohei Mitani

    Bioscience, biotechnology, and biochemistry 70 (12) 3084-7 2006/12

    ISSN: 0916-8451

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    The insulin/insulin-like growth factor-I signaling (IIS) pathway regulates larval diapause, adult lifespan, fat metabolism, and stress-resistance in the nematode Caenorhabditis elegans. One of 38 C. elegans insulin-like genes, ins-11, was disrupted and phenotypic analyses of the gene-disrupted animal were performed. The gene-disruption exhibited a significant influence on the adult lifespan. It antagonized the lifespan extension induced by RNAi knockdown of another insulin-like gene, ins-7. Hence ins-11 appears to be necessary for lifespan extension caused by a decrease in the IIS pathway. This is the first description of gene-disruption of the C. elegans insulin-like gene that suppresses the lifespan extension.

  54. An efficient transgenic system by TA cloning vectors and RNAi for C. elegans. International-journal Peer-reviewed

    Keiko Gengyo-Ando, Sawako Yoshina, Hideshi Inoue, Shohei Mitani

    Biochemical and biophysical research communications 349 (4) 1345-50 2006/11/03

    ISSN: 0006-291X

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    In the nematode, transgenic analyses have been performed by microinjection of DNA from various sources into the syncytium gonad. To expedite these transgenic analyses, we solved two potential problems in this work. First, we constructed an efficient TA-cloning vector system which is useful for any promoter. By amplifying the genomic DNA fragments which contain regulatory sequences with or without the coding region, we could easily construct plasmids expressing fluorescent protein fusion without considering restriction sites. We could dissect motor neurons with three colors in a single animal. Second, we used feeding RNAi to isolate transgenic strains which express lag-2::venus fusion gene. We found that the fusion protein is toxic when ectopically expressed in embryos but is functional to rescue a loss of function mutant in the lag-2 gene. Thus, the transgenic system described here should be useful to examine the protein function in the nematode.

  55. Essential roles of 3'-phosphoadenosine 5'-phosphosulfate synthase in embryonic and larval development of the nematode Caenorhabditis elegans. International-journal Peer-reviewed

    Katsufumi Dejima, Akira Seko, Katsuko Yamashita, Keiko Gengyo-Ando, Shohei Mitani, Tomomi Izumikawa, Hiroshi Kitagawa, Kazuyuki Sugahara, Souhei Mizuguchi, Kazuya Nomura

    The Journal of biological chemistry 281 (16) 11431-40 2006/04/21

    ISSN: 0021-9258

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    Sulfation of biomolecules, which is widely observed from bacteria to humans, plays critical roles in many biological processes. All sulfation reactions in all organisms require activated sulfate, 3'-phosphoadenosine 5'-phosphosulfate (PAPS), as a universal donor. In animals, PAPS is synthesized from ATP and inorganic sulfate by the bifunctional enzyme, PAPS synthase. In mammals, genetic defects in PAPS synthase 2, one of two PAPS synthase isozymes, cause dwarfism disorder, but little is known about the consequences of the complete loss of PAPS synthesis. To define the developmental role of sulfation, we cloned a Caenorhabditis elegans PAPS synthase-homologous gene, pps-1, and depleted expression of its product by isolating the deletion mutant and by RNA-mediated interference. PPS-1 protein exhibits specific activity to form PAPS in vitro, and disruption of the pps-1 gene by RNAi causes pleiotropic developmental defects in muscle patterning and epithelial cell shape changes with a decrease in glycosaminoglycan sulfation. Additionally, the pps-1 null mutant exhibits larval lethality. These data suggest that sulfation is essential for normal growth and integrity of epidermis in C. elegans. Furthermore, reporter analysis showed that pps-1 is expressed in the epidermis and several gland cells but not in neurons and muscles, indicating that PAPS in the neurons and muscles is provided by other cells.

  56. Familial Parkinson mutant alpha-synuclein causes dopamine neuron dysfunction in transgenic Caenorhabditis elegans. International-journal Peer-reviewed

    Tomoki Kuwahara, Akihiko Koyama, Keiko Gengyo-Ando, Mayumi Masuda, Hisatomo Kowa, Makoto Tsunoda, Shohei Mitani, Takeshi Iwatsubo

    The Journal of biological chemistry 281 (1) 334-40 2006/01/06

    ISSN: 0021-9258

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    Mutations in alpha-synuclein gene cause familial form of Parkinson disease, and deposition of wild-type alpha-synuclein as Lewy bodies occurs as a hallmark lesion of sporadic Parkinson disease and dementia with Lewy bodies, implicating alpha-synuclein in the pathogenesis of Parkinson disease and related neurodegenerative diseases. Dopamine neurons in substantia nigra are the major site of neurodegeneration associated with alpha-synuclein deposition in Parkinson disease. Here we establish transgenic Caenorhabditis elegans (TG worms) that overexpresses wild-type or familial Parkinson mutant human alpha-synuclein in dopamine neurons. The TG worms exhibit accumulation of alpha-synuclein in the cell bodies and neurites of dopamine neurons, and EGFP labeling of dendrites is often diminished in TG worms expressing familial Parkinson disease-linked A30P or A53T mutant alpha-synuclein, without overt loss of neuronal cell bodies. Notably, TG worms expressing A30P or A53T mutant alpha-synuclein show failure in modulation of locomotory rate in response to food, which has been attributed to the function of dopamine neurons. This behavioral abnormality was accompanied by a reduction in neuronal dopamine content and was treatable by administration of dopamine. These phenotypes were not seen upon expression of beta-synuclein. The present TG worms exhibit dopamine neuron-specific dysfunction caused by accumulation of alpha-synuclein, which would be relevant to the genetic and compound screenings aiming at the elucidation of pathological cascade and therapeutic strategies for Parkinson disease.

  57. Progressive neurodegeneration in C. elegans model of tauopathy. International-journal Peer-reviewed

    Tomohiro Miyasaka, Zhen Ding, Keiko Gengyo-Ando, Miho Oue, Haruyasu Yamaguchi, Shohei Mitani, Yasuo Ihara

    Neurobiology of disease 20 (2) 372-83 2005/11

    ISSN: 0969-9961

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    Discovery of various mutations in the tau gene among frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) families suggests gain-of-toxic function of wild-type or mutant tau as the mechanism for extensive neuronal loss. We thus generated transgenic nematode (Caenorhabditis elegans) expressing wild-type or mutant (P301L and R406W) tau in the touch (mechanosensory) neurons. Whereas the worm expressing wild-type tau showed a small decrease in the touch response across the lifespan, the worm expressing mutant tau displayed a large and progressive decrease. When the touch neurons lost their function, neuritic abnormalities were found prominent, and microtubular loss became remarkable in the later stage. A substantial fraction of degenerating neurons developed tau accumulation in the cell body and neuronal processes. This neuronal dysfunction is not related to the apoptotic process because little recovery from touch abnormality was observed in the ced-3 or ced-4-deficient background. Expression of GSK3 brought about slight deterioration in the touch response, while expression of HSP70 led to some improvement.

  58. Control of body size by SMA-5, a homolog of MAP kinase BMK1/ERK5, in C. elegans. International-journal Peer-reviewed

    Naoharu Watanabe, Yasuko Nagamatsu, Keiko Gengyo-Ando, Shohei Mitani, Yasumi Ohshima

    Development (Cambridge, England) 132 (14) 3175-84 2005/07

    ISSN: 0950-1991

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    We have analyzed the sma-5(n678) mutant in C. elegans to elucidate mechanisms controlling body size. The sma-5 mutant is very small, grows slowly and its intestinal granules look abnormal. We found a 15 kb deletion in the mutant that includes a 226 bp deletion of the 3' end of the W06B3.2-coding sequence. Based on this result, rescue experiments, RNAi experiments and a newly isolated deletion mutant of W06B3.2, we conclude that W06B3.2 is the sma-5 gene. The sma-5 mutant has much smaller intestine, body wall muscles and hypodermis than those of the wild type. However, the number of intestinal cells or body wall muscle cells is not changed, indicating that the sma-5 mutant has much smaller cells. In relation to the smaller cell size, the amount of total protein is drastically decreased; however, the DNA content of the intestinal nuclei is unchanged in the sma-5 mutant. The sma-5 gene is expressed in intestine, excretory cell and hypodermis, and encodes homologs of a mammalian MAP kinase BMK1/ERK5/MAPK7, which was reported to control cell cycle and cell proliferation. Expression of the sma-5 gene in hypodermis is important for body size control, and it can function both organ-autonomously and non-autonomously. We propose that the sma-5 gene functions in a MAP kinase pathway to regulate body size mainly through control of cell growth.

  59. Nematode chondroitin polymerizing factor showing cell-/organ-specific expression is indispensable for chondroitin synthesis and embryonic cell division. International-journal Peer-reviewed

    Tomomi Izumikawa, Hiroshi Kitagawa, Souhei Mizuguchi, Kazuko H Nomura, Kazuya Nomura, Jun-Ichi Tamura, Keiko Gengyo-Ando, Shohei Mitani, Kazuyuki Sugahara

    The Journal of biological chemistry 279 (51) 53755-61 2004/12/17

    ISSN: 0021-9258

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    Chondroitin polymerization was first demonstrated in vitro when human chondroitin synthase (ChSy) was coexpressed with human chondroitin polymerizing factor (ChPF), which is homologous to ChSy but has little glycosyltransferase activity. To analyze the biological function of chondroitin, the Caenorhabditis elegans ortholog of human ChSy (sqv-5) was recently cloned, and the expression of its product was depleted by RNA-mediated interference (RNAi) and deletion mutagenesis. Blocking of chondroitin synthesis resulted in defects of cytokinesis in early embryogenesis, and eventually, cell division stopped. Here, we cloned the ortholog of human ChPF in C. elegans, PAR2.4. Despite little glycosyltransferase activity of the gene product, chondroitin polymerization was demonstrated as in the case of mammals when PAR2.4 was coexpressed with cChSy in vitro. The worm phenotypes including the reversion of cytokinesis, observed after the depletion of PAR2.4 by RNAi, were very similar to the cChSy (sqv-5)-RNAi phenotypes. Thus, PAR2.4 in addition to cChSy is indispensable for the biosynthesis of chondroitin in C. elegans, and the two cooperate to synthesize chondroitin in vivo. The expression of the PAR2.4 protein was observed in seam cells, which can act as neural stem cells in early embryonic lineages. The expression was also detected in vulva and distal tip cells of the growing gonad arms from L3 through to the young adult stage. These findings are consistent with the notion that chondroitin is involved in the organogenesis of the vulva and maturation of the gonad and also indicative of an involvement in distal tip cell migration and neural development.

  60. The Caenorhabditis elegans eukaryotic initiation factor 5A homologue, IFF-1, is required for germ cell proliferation, gametogenesis and localization of the P-granule component PGL-1. International-journal Peer-reviewed

    Momoyo Hanazawa, Ichiro Kawasaki, Hirofumi Kunitomo, Keiko Gengyo-Ando, Karen L Bennett, Shohei Mitani, Yuichi Iino

    Mechanisms of development 121 (3) 213-24 2004/03

    ISSN: 0925-4773

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    Eukaryotic initiation factor 5A (eIF-5A) was originally isolated as a translation initiation factor. However, this function has since been reconsidered, with recent studies pointing to roles for eIF-5A in mRNA metabolism and trafficking [Microbiol. Mol. Biol. Rev. 66 (2002) 460; Eur. Mol. Biol. Org. J. 17 (1998) 2914]. The Caenorhabditis elegans genome contains two eIF-5A homologues, iff-1 and iff-2, whose functions in vivo were examined in this study. The iff-2 mutation causes somatic defects that include slow larval growth and disorganized somatic gonadal structures in hermaphrodites. iff-2 males show disorganized tail sensory rays and spicules. On the other hand, iff-1 mRNA is expressed in the gonad, and the lack of iff-1 activity causes sterility with an underproliferated germline resulting from impaired mitotic proliferation in both hermaphrodites and males. In spite of underproliferation, meiotic nuclei are observed, as revealed by presence of immunoreactivity to the anti-HIM-3 antibody; however, no gametogenesis occurs in the iff-1 gonads. These phenotypes are in part similar to the mutants affected in the components of P granules, which are the C. elegans counterparts of germ granules [Curr. Top Dev. Biol. 50 (2000) 155]. We found that localization of the P-granule component PGL-1 to P granules is disrupted in the iff-1 mutant. In summary, the two C. elegans homologues of eIF-5A act in different tissues: IFF-2 is required in the soma, and IFF-1 is required in the germline for germ cell proliferation, for gametogenesis after entry into meiosis, and for proper PGL-1 localization on P granules.

  61. Cell corpse engulfment mediated by C. elegans phosphatidylserine receptor through CED-5 and CED-12. International-journal Peer-reviewed

    Xiaochen Wang, Yi-Chun Wu, Valerie A Fadok, Ming-Chia Lee, Keiko Gengyo-Ando, Li-Chun Cheng, Duncan Ledwich, Pei-Ken Hsu, Jia-Yun Chen, Bin-Kuan Chou, Peter Henson, Shohei Mitani, Ding Xue

    Science (New York, N.Y.) 302 (5650) 1563-6 2003/11/28

    eISSN: 1095-9203

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    During apoptosis, phosphatidylserine, which is normally restricted to the inner leaflet of the plasma membrane, is exposed on the surface of apoptotic cells and has been suggested to act as an "eat-me" signal to trigger phagocytosis. It is unclear how phagocytes recognize phosphatidylserine. Recently, a putative phosphatidylserine receptor (PSR) was identified and proposed to mediate recognition of phosphatidylserine and phagocytosis. We report that psr-1, the Caenorhabditis elegans homolog of PSR, is important for cell corpse engulfment. In vitro PSR-1 binds preferentially phosphatidylserine or cells with exposed phosphatidylserine. In C. elegans, PSR-1 acts in the same cell corpse engulfment pathway mediated by intracellular signaling molecules CED-2 (homologous to the human CrkII protein), CED-5 (DOCK180), CED-10 (Rac GTPase), and CED-12 (ELMO), possibly through direct interaction with CED-5 and CED-12. Our findings suggest that PSR-1 is likely an upstream receptor for the signaling pathway containing CED-2, CED-5, CED-10, and CED-12 proteins and plays an important role in recognizing phosphatidylserine during phagocytosis.

  62. Translational control of maternal glp-1 mRNA by POS-1 and its interacting protein SPN-4 in Caenorhabditis elegans. International-journal Peer-reviewed

    Ken-Ichi Ogura, Norihito Kishimoto, Shohei Mitani, Keiko Gengyo-Ando, Yuji Kohara

    Development (Cambridge, England) 130 (11) 2495-503 2003/06

    ISSN: 0950-1991

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    The translation of maternal glp-1 mRNAs is regulated temporally and spatially in C. elegans embryos. The 3' UTR (untranslated region) of the maternal glp-1 mRNA is important for both kinds of regulation. The spatial control region is required to suppress translation in the posterior blastomeres. The temporal one is required to suppress translation in oocytes and one-cell stage embryos. We show that a CCCH zinc-finger protein, POS-1, represses glp-1 mRNA translation by binding to the spatial control region. We identified an RNP-type RNA-binding protein, SPN-4, as a POS-1-interacting protein. SPN-4 is present developmentally from the oocyte to the early embryo and its distribution overlaps with that of POS-1 in the cytoplasm and P granules of the posterior blastomeres. SPN-4 binds to a subregion of the temporal control region in the 3' UTR and is required for the translation of glp-1 mRNA in the anterior blastomeres. We propose that the balance between POS-1 and SPN-4 controls the translation of maternal glp-1 mRNA.

  63. Chondroitin proteoglycans are involved in cell division of Caenorhabditis elegans. International-journal Peer-reviewed

    Souhei Mizuguchi, Toru Uyama, Hiroshi Kitagawa, Kazuko H Nomura, Katsufumi Dejima, Keiko Gengyo-Ando, Shohei Mitani, Kazuyuki Sugahara, Kazuya Nomura

    Nature 423 (6938) 443-8 2003/05/22

    ISSN: 0028-0836

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    Glycosaminoglycans such as heparan sulphate and chondroitin sulphate are extracellular sugar chains involved in intercellular signalling. Disruptions of genes encoding enzymes that mediate glycosaminoglycan biosynthesis have severe consequences in Drosophila and mice. Mutations in the Drosophila gene sugarless, which encodes a UDP-glucose dehydrogenase, impairs developmental signalling through the Wnt family member Wingless, and signalling by the fibroblast growth factor and Hedgehog pathways. Heparan sulphate is involved in these pathways, but little is known about the involvement of chondroitin. Undersulphated and oversulphated chondroitin sulphate chains have been implicated in other biological processes, however, including adhesion of erythrocytes infected with malaria parasite to human placenta and regulation of neural development. To investigate chondroitin functions, we cloned a chondroitin synthase homologue of Caenorhabditis elegans and depleted expression of its product by RNA-mediated interference and deletion mutagenesis. Here we report that blocking chondroitin synthesis results in cytokinesis defects in early embryogenesis. Reversion of cytokinesis is often observed in chondroitin-depleted embryos, and cell division eventually stops, resulting in early embryonic death. Our findings show that chondroitin is required for embryonic cytokinesis and cell division.

  64. A CaMK cascade activates CRE-mediated transcription in neurons of Caenorhabditis elegans. International-journal Peer-reviewed

    Yoshishige Kimura, Ethan E Corcoran, Koh Eto, Keiko Gengyo-Ando, Masa-Aki Muramatsu, Ryoji Kobayashi, Jonathan H Freedman, Shohei Mitani, Masatoshi Hagiwara, Anthony R Means, Hiroshi Tokumitsu

    EMBO reports 3 (10) 962-6 2002/10

    ISSN: 1469-221X

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    Calcium (Ca2+) signals regulate a diverse set of cellular responses, from proliferation to muscular contraction and neuro-endocrine secretion. The ubiquitous Ca2+ sensor, calmodulin (CaM), translates changes in local intracellular Ca2+ concentrations into changes in enzyme activities. Among its targets, the Ca2+/CaM-dependent protein kinases I and IV (CaMKs) are capable of transducing intraneuronal signals, and these kinases are implicated in neuronal gene regulation that mediates synaptic plasticity in mammals. Recently, the cyclic AMP response element binding protein (CREB) has been proposed as a target for a CaMK cascade involving not only CaMKI or CaMKIV, but also an upstream kinase kinase that is also CaM regulated (CaMKK). Here, we report that all components of this pathway are coexpressed in head neurons of Caenorhabditis elegans. Utilizing a transgenic approach to visualize CREB-dependent transcription in vivo, we show that this CaMK cascade regulates CRE-mediated transcription in a subset of head neurons in living nematodes.

  65. HEN-1, a secretory protein with an LDL receptor motif, regulates sensory integration and learning in Caenorhabditis elegans. International-journal Peer-reviewed

    Takeshi Ishihara, Yuichi Iino, Akiko Mohri, Ikue Mori, Keiko Gengyo-Ando, Shohei Mitani, Isao Katsura

    Cell 109 (5) 639-49 2002/05/31

    ISSN: 0092-8674

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    Animals sense many environmental stimuli simultaneously and integrate various sensory signals within the nervous system both to generate proper behavioral responses and also to form relevant memories. HEN-1, a secretory protein with an LDL receptor motif, regulates such processes in Caenorhabditis elegans. The hen-1 mutants show defects in the integration of two sensory signals and in behavioral plasticity by paired stimuli, although their sensation capability seems to be identical to that of the wild-type. The HEN-1 protein is expressed in two pairs of neurons, but expression in other neurons is sufficient for wild-type behavior. In addition, expression of HEN-1 at the adult stage is sufficient. Thus, HEN-1 regulates sensory processing non-cell-autonomously in the mature neuronal circuit.

  66. Caenorhabditis elegans reticulon interacts with RME-1 during embryogenesis. International-journal Peer-reviewed

    Jun Iwahashi, Ichiro Kawasaki, Yuji Kohara, Keiko Gengyo-Ando, Shohei Mitani, Yasumi Ohshima, Nobuyuki Hamada, Koyu Hara, Takahito Kashiwagi, Tetsuya Toyoda

    Biochemical and biophysical research communications 293 (2) 698-704 2002/05/03

    ISSN: 0006-291X

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    Reticulon (RTN) family proteins are localized in the endoplasmic reticulum (ER). At least four different RTN genes have been identified in mammals, but in most cases, the functions of the encoded proteins except mammalian RTN4-A and RTN4-B are unknown. Each RTN gene produces 1-3 proteins by different promoters and alternative splicing. In Caenorhabditis elegans, there is a single gene (rtn gene) encoding three reticulon proteins, nRTN-A, B, and C. mRNA of nRTN-C is expressed in germ cells and embryos. However, nRTN-C protein is only expressed during embryogenesis and rapidly disappears after hatch. By yeast two-hybrid screening, two clones encoding the same C-terminal region of RME-1, a protein functioning in the endocytic recycling, were isolated. These findings suggest that nRTN-C functions in the endocytic pathway during embryogenesis.

  67. C. elegans slit acts in midline, dorsal-ventral, and anterior-posterior guidance via the SAX-3/Robo receptor. International-journal Peer-reviewed

    J C Hao, T W Yu, K Fujisawa, J G Culotti, K Gengyo-Ando, S Mitani, G Moulder, R Barstead, M Tessier-Lavigne, C I Bargmann

    Neuron 32 (1) 25-38 2001/10/11

    ISSN: 0896-6273

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    Robo receptors interact with ligands of the Slit family. The nematode C. elegans has one Robo receptor (SAX-3) and one Slit protein (SLT-1), which direct ventral axon guidance and guidance at the midline. In larvae, slt-1 expression in dorsal muscles repels axons to promote ventral guidance. SLT-1 acts through the SAX-3 receptor, in parallel with the ventral attractant UNC-6 (Netrin). Removing both UNC-6 and SLT-1 eliminates all ventral guidance information for some axons, revealing an underlying longitudinal guidance pathway. In the embryo, slt-1 is expressed at high levels in anterior epidermis. Embryonic expression of SLT-1 provides anterior-posterior guidance information to migrating CAN neurons. Surprisingly, slt-1 mutants do not exhibit the nerve ring and epithelial defects of sax-3 mutants, suggesting that SAX-3 has both Slit-dependent and Slit-independent functions in development.

  68. Characterization of mutations induced by ethyl methanesulfonate, UV, and trimethylpsoralen in the nematode Caenorhabditis elegans. International-journal Peer-reviewed

    K Gengyo-Ando, S Mitani

    Biochemical and biophysical research communications 269 (1) 64-9 2000/03/05

    ISSN: 0006-291X

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    The genome project of the nematode Caenorhabditis elegans is completed. It is important and useful to disrupt nematode genes to know their function. We treated wild-type animals with potential candidates for mutagens for reverse genetics, EMS (ethyl methanesulfonate), short-wavelength UV, and long-wavelength UV in the presence of TMP (trimethylpsoralen). We estimated forward mutation rates by counting the occurrence of a marker unc-22 mutation. We found that the forward mutation rate by TMP/UV could be comparable with EMS by improving the frequency one order higher than before. We next isolated mutants of another marker gene ben-1 and examined the probability for the deletion mutations by PCR and sequencing. Deletion mutations were found only by TMP/UV method, which suggested TMP/UV is the choice for deletion mutagenesis among these methods. As a pilot experiment, we could isolate actual deletion mutations at a much higher frequency than previously.

  69. A murine neural-specific homolog corrects cholinergic defects in Caenorhabditis elegans unc-18 mutants Peer-reviewed

    K GengyoAndo, H Kitayama, M Mukaida, Y Ikawa

    JOURNAL OF NEUROSCIENCE 16 (21) 6695-6702 1996/11

    ISSN: 0270-6474

  70. The C. elegans unc-18 gene encodes a protein expressed in motor neurons Peer-reviewed

    Keiko Gengyo-Ando, Yasuko Kamiya, Ayanori Yamakawa, Ken-ichi Kodaira, Kiyoji Nishiwaki, Johji Miwa, Isao Hori, Ryuji Hosono

    Neuron 11 (4) 703-711 1993/10

    DOI: 10.1016/0896-6273(93)90080-b  

    ISSN: 0896-6273

  71. Single charge change on the helical surface of the paramyosin rod dramatically disrupts thick filament assembly in Caenorhabditis elegans. International-journal Peer-reviewed

    K Gengyo-Ando, H Kagawa

    Journal of molecular biology 219 (3) 429-41 1991/06/05

    DOI: 10.1016/0022-2836(91)90184-8  

    ISSN: 0022-2836

  72. Paramyosin gene (unc-15) of Caenorhabditis elegans Peer-reviewed

    Hiroaki Kagawa, Keiko Gengyo, Andrew D. Mclachlan, Sydney Brenner, Jonathan Karn

    Journal of Molecular Biology 207 (2) 311-333 1989/05

    DOI: 10.1016/0022-2836(89)90257-x  

    ISSN: 0022-2836

  73. Frequency-Regulated Repeated Micro-Vibration Promotes Osteoblast Differentiation Through BMP Signaling in MC3T3-E1 Cells Peer-reviewed

    Ayumu Matsushita, Tada-aki Kudo, Kanako Tominami, Yohei Hayashi, Takuya Noguchi, Takakuni Tanaka, Satoshi Izumi, Keiko Gengyo-Ando, Atsushi Matsuzawa, Guang Hong, Junichi Nakai

    Life 15 (4) 588-588 2025/04/03

    Publisher: MDPI AG

    DOI: 10.3390/life15040588  

    eISSN: 2075-1729

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    Physical stimulation, which is a key factor affecting the metabolism of osteoblasts and their precursor cells, plays an important role in bone remodeling; however, the role of micro-vibrations in osteoblast differentiation is unclear. In the present study, we determined the effects of frequency-regulated repeated micro-vibration (FRMV) on cell proliferation and established a method to induce osteoblast differentiation through FRMV using the mouse pre-osteoblast-like cell line MC3T3-E1, which is widely used in bone metabolism research. The results indicated that FRMV significantly influenced the proliferation of MC3T3-E1 cells in a normal growth medium. FRMV at 42.2 Hz significantly promoted proliferation, whereas FRMV at 92.1 Hz showed no effect on the proliferation rate. Moreover, FRMV at 42.2 Hz significantly increased alkaline phosphatase (ALP) enzyme activity and ALP gene expression in MC3T3-E1 cells. Treatment with LDN193189, a bone morphogenetic protein (BMP) signaling inhibitor, revealed that the FRMV-induced upregulation in ALP enzyme activity and ALP gene expression were significantly suppressed in MC3T3-E1 cells. The results suggest that the FRMV protocol developed in the present study induces osteoblast differentiation through the BMP signaling pathway. Thus, FRMV may contribute to the development of effective bone regeneration technologies.

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    安藤恵子

    月刊細胞 57 (2) 2025

    ISSN: 1346-7557

  2. in vivo functional imaging with genetically encoded calcium indicator G-CaMP

    中井淳一, 安藤恵子, 佐藤正晃, 大倉正道

    Journal of Oral Biosciences Supplement (Web) 2020 2020

    ISSN: 2187-9109

  3. 線虫遺伝学を用いたヒト相同遺伝子の機能解析

    三谷 昌平, 吉名 佐和子, 堀 沙耶香, 末廣 勇司, 出嶋 克史, 岩田 悟, 中台 枝里子, 安藤 恵子, 本橋 智子

    東京女子医科大学総合研究所紀要 36 24-25 2017/02

    Publisher: 東京女子医科大学総合研究所

    ISSN: 0911-4491

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    野村和子, 藤井潤, 宮崎清香, 村田大輔, 村田大輔, 村田大輔, 秋好紗弥香, 松田采子, 力武茉莉花, 瀬川孝耶, 沖野望, 伊東信, 安藤恵子, 岩淵和久, 田代康介, 野村一也, 野村一也

    日本糖質学会年会要旨集 36th 2017

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    日本糖質学会年会要旨集 36th 2017

  6. 生殖幹細胞の自己複製に必要な線虫C.elegans GPIアンカー型タンパク質の解析

    力武茉莉花, 松田采子, 村田大輔, 村田大輔, 村田大輔, 出嶋克史, 出嶋克史, 出嶋克史, 野村和子, 野村和子, 三谷昌平, 三谷昌平, 安藤恵子, 安藤恵子, 安藤恵子, 中台枝里子, 中台枝里子, 田代康介, 野村一也, 野村一也

    日本糖質学会年会要旨集 36th 2017

  7. G-CaMP7発現マウスを用いた大脳皮質神経活動のミクロ、マクロ解析法

    茂木 優貴, 安藤 恵子, 沖 篤志, 岩井 陽一, 毛内 拡, 平瀬 肇, 大倉 正道, 中井 淳一

    日本生理学雑誌 78 (3) 56-56 2016/05

    Publisher: (一社)日本生理学会

    ISSN: 0031-9341

  8. CDG(先天性グリコシル化異常症Congenital Disorders of Glycosylation)モデル生物としての線虫の有用性-DPAGT1(ALG7)遺伝子破壊株を中心とした解析

    金氣菜々子, 松田采子, 出嶋克史, 出嶋克史, 出嶋克史, 村田大輔, 村田大輔, 村田大輔, 野村和子, 野村和子, 三谷昌平, 三谷昌平, 安藤恵子, 安藤恵子, 安藤恵子, 大倉隆司, 野村一也, 野村一也

    日本分子生物学会年会プログラム・要旨集(Web) 39th 2016

  9. 線虫C.elegansにおけるアセチルCoAトランスポーターの機能解析

    任建宇, 村田大輔, 村田大輔, 村田大輔, 野村和子, 野村和子, 三谷昌平, 三谷昌平, 安藤恵子, 安藤恵子, 安藤恵子, 田代康介, 平林義雄, 金井好克, PHETDEE Kanokporn, 野村一也, 野村一也

    日本分子生物学会年会プログラム・要旨集(Web) 39th 2016

  10. 生殖幹細胞の自己複製に必要な線虫C.elegans GPIアンカー型タンパク質の解析

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    日本分子生物学会年会プログラム・要旨集(Web) 39th 2016

  11. G‐CaMP7発現マウス大脳皮質脳細胞活動の細胞‐領野スケール長期イメージング実験解析法

    茂木優貴, 茂木優貴, 安藤恵子, 安藤恵子, 沖篤志, 沖篤志, 岩井陽一, 毛内拡, 平瀬肇, 平瀬肇, 平瀬肇, 大倉正道, 大倉正道, 中井淳一, 中井淳一

    日本生化学会大会(Web) 88th 1LBA113 (WEB ONLY)-[1LBA113] 2015/12

    Publisher: (公社)日本生化学会

  12. G-CaMP7発現マウス大脳皮質脳細胞活動の細胞-領野スケール長期イメージング実験解析法

    茂木 優貴, 安藤 恵子, 沖 篤志, 岩井 陽一, 毛内 拡, 平瀬 肇, 大倉 正道, 中井 淳一

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集 88回・38回 [1LBA113]-[1LBA113] 2015/12

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  13. CDG(先天性グリコシル化異常症Congenital Disorders of Glycosylation)モデル生物としての線虫C.elegansの有用性 DPAGT1(ALG7)遺伝子破壊株を中心とした解析

    野村 一也, 松田 采子, 金氣 菜々子, 出嶋 克史, 村田 大輔, 野村 和子, 三谷 昌平, 安藤 恵子, 大倉 隆司

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    安藤 恵子, 中井 淳一

    生体の科学 66 (5) 388-389 2015/10

    Publisher: (公財)金原一郎記念医学医療振興財団

    ISSN: 0370-9531

  15. Rational design of a high-affinity, fast, red calcium indicator R-CaMP2

    Masatoshi Inoue, Atsuya Takeuchi, Shin-ichiro Horigane, Masamichi Ohkura, Keiko Gengyo-Ando, Hajime Fujii, Satoshi Kamijo, Sayaka Takemoto-Kimura, Masanobu Kano, Junichi Nakai, Kazuo Kitamura, Haruhiko Bito

    JOURNAL OF PHARMACOLOGICAL SCIENCES 128 (3) S92-S92 2015/07

    ISSN: 1347-8613

    eISSN: 1347-8648

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    岩瀬奏絵, 永村ゆう子, 中井淳一, 安藤恵子, 岩瀬奏絵, 永村ゆう子, 中井淳一, 安藤恵子

    日本薬理学会関東部会プログラム・要旨集 133rd 2015

  17. 受精前後における細胞内膜系リモデリングの時空間的制御機構

    坂口愛沙, 佐藤美由紀, 佐藤克哉, 安藤恵子, 中井淳一, 前島郁子, 原太一, 依光朋宏, 佐藤健, 佐藤健

    日本生化学会大会(Web) 88th 2015

  18. G-CaMP7を大脳皮質に発現するマウスを用いた神経活動のミクロ,マクロ解析法

    茂木優貴, 茂木優貴, 安藤恵子, 安藤恵子, 沖篤志, 沖篤志, 岩井陽一, 毛内拡, 平瀬肇, 平瀬肇, 平瀬肇, 大倉正道, 大倉正道, 中井淳一, 中井淳一

    日本薬理学会関東部会プログラム・要旨集 132nd 2015

  19. 生体膜を利用した細胞内外物質の処理による生体恒常性の維持 メンブレントラフィックにおけるSec1/Munc18ファミリーの機能と疾患

    安藤 恵子

    日本生化学会大会プログラム・講演要旨集 87回 [4S06p-4] 2014/10

    Publisher: (公社)日本生化学会

  20. 線虫C.elegans糖鎖遺伝子機能の網羅的スクリーニングとデータベース化 C.elegans GlycoGene Database(CGGDB)の作製

    秋好 紗弥香, 野村 和子, 出嶋 克史, 村田 大輔, 松田 采子, 金氣 菜々子, 安藤 恵子, 吉名 佐和子, 三谷 昌平, 鈴木 芳典, 鹿内 俊秀, 成松 久, 野村 一也

    日本生化学会大会プログラム・講演要旨集 87回 [3T16a-02] 2014/10

    Publisher: (公社)日本生化学会

  21. 蛍光カルシウムプローブG‐CaMPによるin vivoカルシウムイメージング

    中井淳一, 大倉正道, 安藤恵子

    日本薬学会関東支部大会講演要旨集 58th 82 2014/09/30

  22. 線虫受精卵においてダイナミックに変化するRAB-11の動態制御機構の解析

    坂口 愛沙, 佐藤 美由紀, 安藤 恵子, 佐藤 克哉, 中井 淳一, 佐藤 健

    日本細胞生物学会大会講演要旨集 66回 117-117 2014/05

    Publisher: (一社)日本細胞生物学会

  23. 個体(線虫)レベルでの超多並列刺激応答モニターシステム

    藤泰一, 高橋尚也, 安藤恵子, 大倉正道, 中井淳一, 西垣功一

    日本分子生物学会年会プログラム・要旨集(Web) 37th 2014

  24. 低分子量GTPase RAB-11の新規結合因子REI-1/REI-2は受精後のRAB-11再局在化を制御する

    坂口愛沙, 佐藤美由紀, 安藤恵子, 佐藤克哉, 中井淳一, 佐藤健

    日本分子生物学会年会プログラム・要旨集(Web) 37th 2014

  25. ファゴリソソーム形成における低分子量Gタンパク質ARL8の機能解析

    橋本 圭介, 長澤 茉耶, 阿部 芙実子, 安藤 恵子, 三谷 昌平, 紺谷 圏二, 堅田 利明

    日本生化学会大会プログラム・講演要旨集 86回 2P-212 2013/09

    Publisher: (公社)日本生化学会

  26. 線虫による香気評価の検討

    松永祐, 藤田孝, 清宮はるな, 安藤恵子, 中井淳一, 長谷川登志夫

    香料・テルペンおよび精油化学に関する討論会講演要旨集 57th 2013

  27. 受精における表層顆粒分泌の制御因子RAB-11に結合する新規因子の解析

    坂口愛沙, 佐藤美由紀, 安藤恵子, 佐藤克哉, 中井淳一, 佐藤健

    日本分子生物学会年会プログラム・要旨集(Web) 36th 2013

  28. 線虫C.elegansの生殖系列細胞におけるGPIアンカー型タンパク質の解析

    松田采子, 村田大輔, 村田大輔, 野村和子, 野村和子, 秋好紗弥香, 出嶋克史, 出嶋克史, 出嶋克史, WELLS Lance, ABBOTT Karen L., 川崎ナナ, 川崎ナナ, 安藤恵子, 安藤恵子, 安藤恵子, 中台枝里子, 三谷昌平, 三谷昌平, 野村一也, 野村一也

    日本分子生物学会年会プログラム・要旨集(Web) 36th 2013

  29. スフィンゴ糖脂質合成酵素の遺伝子破壊による線虫寿命の延長メカニズム

    野村和子, 宮崎清香, 秋好紗弥香, 松田采子, 中台枝里子, 三谷昌平, 安藤恵子, 平林義雄, 野村一也

    日本生化学会大会(Web) 86th 2013

  30. Imaging of neuronal activities at the single-cell and the single-synapse levels using high-sensitivity and fast-responsivity G-CaMP-type genetically encoded calcium indicators

    Masamichi Ohkura, Junko Sadakari, Takuya Sasaki, Keiko Gengyo-Ando, Yuko Kagawa-Nagamura, Chiaki Kobayashi, Yuji Ikegaya, Junichi Nakai

    JOURNAL OF PHARMACOLOGICAL SCIENCES 121 129P-129P 2013

    ISSN: 1347-8613

  31. 難治性てんかんの責任遺伝子Munc18‐1変異の機能解析

    大澤明香音, 安藤恵子, 永村ゆう子, 大倉正道, 中井淳一

    日本分子生物学会年会プログラム・要旨集(Web) 36th WEB ONLY 1P-0915 2013

  32. GPIアンカー合成は線虫Caenorhabditis elegansの配偶子幹細胞ニッチの維持と生殖系列細胞発生に必須である

    村田 大輔, 野村 和子, 出嶋 克史, 水口 惣平, 川崎 ナナ, 中島 紫, 伊藤 さつき, 安藤 恵子, 中台 枝里子, 三谷 昌平, 松田 采子, 野村 一也

    日本生化学会大会プログラム・講演要旨集 85回 3T25-07 2012/12

    Publisher: (公社)日本生化学会

  33. GPIアンカー型蛋白質の生合成は線虫C.elegansの生殖細胞発生に必須である

    村田 大輔, 野村 和子, 出嶋 克史, 水口 惣平, 川崎 ナナ, 中島 紫, 伊東 さつき, 安藤 恵子, 中台 枝理子, 三谷 昌平, 野村 一也

    脂質生化学研究 54 133-134 2012/05

    Publisher: 日本脂質生化学会

    ISSN: 0285-1520

  34. 改良型G-CaMPを用いた線虫運動出力系の神経調節機構の解明

    宇佐美 篤, 安藤 恵子, 大倉 正道, 池谷 裕二, 中井 淳一, 松木 則夫

    日本薬学会年会要旨集 132年会 (3) 117-117 2012/03

    Publisher: (公社)日本薬学会

    ISSN: 0918-9823

  35. 香りの評価法の検討-バイオアッセイを用いた香り評価の試み-

    中井淳一, 永村ゆう子, 大倉正道, 清宮はるな, 藤田孝, 松永祐, 長谷川登志夫, 安藤恵子

    Aroma Research 13 (2) 2012

    ISSN: 1345-4722

  36. 細胞内のタンパク輸送制御機構におけるADAMTS9/GON-1の機能解析

    吉名佐和子, 吉名佐和子, 吉名佐和子, 榊建二郎, 林亜紀, 林亜紀, 林亜紀, 安藤恵子, 安藤恵子, 安藤恵子, 井上英史, 飯野雄一, 三谷昌平, 三谷昌平, 三谷昌平

    臨床ストレス応答学会大会抄録集 7th 2012

  37. マンノシルトランスフェラーゼの生殖巣における機能-線虫糖脂質合成経路において

    野村和子, 宮崎清香, 秋好紗耶香, 殷ろ, 松田采子, 中台枝里子, 三谷昌平, 安藤恵子, 安藤恵子, 平林義雄

    日本分子生物学会年会プログラム・要旨集(Web) 35th 2012

  38. リソソームへの輸送における低分子量Gタンパク質Arl8の機能解析

    紺谷 圏二, 佐々木 文佳, 長澤 茉耶, 安藤 恵子, 三谷 昌平, 堅田 利明

    日本生化学会大会プログラム・講演要旨集 84回 4S13a-1 2011/09

    Publisher: (公社)日本生化学会

    ISSN: 0037-1017

  39. 線虫 C. elegans のスフィンゴ糖脂質合成は卵母細胞の形成と初期胚分裂に必須である

    野村 和子, 林 康弘, 宮崎 清香, 秋好 紗弥香, 村田 大輔, 出嶋 克史, 水口 惣平, 中台 枝理子, 安藤 恵子, 三谷 昌平, 平林 義雄, 伊東 信, 野村 一也

    脂質生化学研究 53 187-187 2011/04/28

    ISSN: 0285-1520

  40. 細胞分裂を制御する線虫糖鎖遺伝子の同定

    野村一也, 野村和子, 林康広, 村田大輔, 出嶋克史, 水口惣平, 安藤恵子, 中臺枝里子, 三谷昌平, 川崎ナナ, 伊藤さつき, 中島紫, 伊東信, 平林義雄

    日本糖質学会年会要旨集 30th 2011

  41. in vivo Ca2+ imagingを用いた線虫運動出力系の調節機構の解明

    宇佐美篤, 安藤恵子, 池谷裕二, 中井淳一, 松木則夫

    次世代を担う創薬・医療薬理シンポジウムプログラム・要旨集 2011 2011

  42. In vivo calcium imaging of C. elegans body wall muscles with genetically encoded calcium probe G-CaMP

    Junichi Nakai, Keiko Gengyo-Ando, Atsushi Usami, Masamichi Ohkura, Yuji Ikegaya, Norio Matsuki

    JOURNAL OF PHARMACOLOGICAL SCIENCES 115 111P-111P 2011

    ISSN: 1347-8613

  43. Dynamic neuromuscular regulation in freely crawling C. elegans: High-resolution and large-scale in vivo Ca2+ imaging

    Atsushi Usami, Keiko Gengyo-Ando, Yuko Nagamura, Yuka Yoshida, Norio Matsuki, Yuji Ikegaya, Junichi Nakai

    NEUROSCIENCE RESEARCH 71 E242-E242 2011

    DOI: 10.1016/j.neures.2011.07.1058  

    ISSN: 0168-0102

  44. 脂質とステロイドのin vivoでの機能 無脊椎動物モデル生体からのアプローチ 多胞体形成にはオキシステロール結合蛋白質(OSBP)関連蛋白質とコレステロールが必要である(Functions of lipids and steroids in vivo: approaches from invertebrate model organisms Multivesicular body formation requires Oxysterol-binding protein (OSBP)-related pr

    小鮒 弘幸, 井上 貴雄, 安藤 恵子, 三谷 昌平, 新井 洋由

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集 83回・33回 1W19-3 2010/12

    Publisher: (公社)日本生化学会

  45. 小胞輸送蛋白質VIP36の機能解析

    福島 慶子, 井手尾 浩子, 安藤 恵子, 三谷 昌平, 出嶋 克史, 野村 一也, 山下 克子

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集 83回・33回 3P-0009 2010/12

    Publisher: (公社)日本生化学会

    ISSN: 0037-1017

  46. 蛍光カルシウムセンサーG-CaMP4を用いたin vivoとin vitroイメージング(In vivo or in vitro imaging of calcium dynamics with genetically encoded sensor G-CaMP4)

    宇佐美 篤, 安藤 恵子, 大倉 正道, 松木 則夫, 池谷 裕二, 中井 淳一

    神経化学 49 (2-3) 772-772 2010/08

    Publisher: 日本神経化学会

    ISSN: 0037-3796

  47. 【Gタンパク質シグナル研究の新展開】 モデル生物線虫から見た低分子量G蛋白質Rab

    安藤 恵子

    細胞 42 (3) 104-107 2010/03

    Publisher: (株)ニュー・サイエンス社

    ISSN: 1346-7557

  48. 生殖腺体細胞におけるGPIアンカー生合成は線虫C.elegansの生殖幹細胞の分裂および胚発生に必須である

    村田大輔, 野村和子, 出嶋克史, 水口惣平, 川崎ナナ, 中島紫, 伊藤さつき, 安藤恵子, 中台枝里子, 三谷昌平, 野村一也

    生化学 2010

    ISSN: 0037-1017

  49. 線虫C.elegansを用いた生体膜脂肪酸環境の感知機構の解析

    平田祐介, 田中陸人, 河野望, 河野望, 井上貴雄, 井上貴雄, 有山博之, 鈴木健裕, 堂前直, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 新井洋由, 新井洋由

    生体膜と薬物の相互作用シンポジウム講演要旨集 32nd 2010

    ISSN: 0919-2131

  50. In vivo or in vitro imaging of calcium dynamics with genetically encoded sensor G-CaMP4

    Atsushi Usami, Keiko Ando, Masamichi Ohkura, Norio Matsuki, Yuji Ikegaya, Junichi Nakai

    NEUROSCIENCE RESEARCH 68 E443-E443 2010

    DOI: 10.1016/j.neures.2010.07.1966  

    ISSN: 0168-0102

  51. FATP family have roles in the surface barrier as very long chain fatty acid acyl-CoA synthetases

    Eriko Kage-Nakadai, Hiroyuki Kobuna, Masako Kimura, Keiko Gengyo-Ando, Takao Inoue, Hiroyuki Arai, Shohei Mitani

    JOURNAL OF PHYSIOLOGICAL SCIENCES 60 S102-S102 2010

    ISSN: 1880-6546

  52. 線虫C.elegansを用いた脂肪酸転移酵素LPIAT2の生理機能の解析

    今江理恵子, 井上貴雄, 原直子, 安藤恵子, 三谷昌平, 新井洋由

    衛生薬学・環境トキシコロジー講演要旨集 2009 146 2009/10/02

    ISSN: 0919-2115

  53. Comprehensive analysis of acyltransferases of de novo glycerolipid synthesis

    櫻木健司, 井上貴雄, 原直子, 今江理恵子, 河野望, 鴻宗義, 安藤恵子, 三谷昌平, 新井洋由

    生化学 ROMBUNNO.2P-185 2009/09/25

    ISSN: 0037-1017

  54. S9セリンプロテアーゼの構造、機能から応用へ 線虫を用いたS9セリンプロテアーゼの生理機能解析

    吉名 佐和子, 安藤 恵子, 飯野 雄一, 井上 英史, 三谷 昌平

    日本生化学会大会プログラム・講演要旨集 82回 1S17a-3 2009/09

    Publisher: (公社)日本生化学会

    ISSN: 0037-1017

  55. 線虫糖脂質結合ガレクチンの細菌感染防御における機能

    井手尾 浩子, 福島 慶子, 安藤 恵子, 三谷 昌平, 出嶋 克史, 野村 一也, 山下 克子

    日本生化学会大会プログラム・講演要旨集 82回 4T9p-15 2009/09

    Publisher: (公社)日本生化学会

    ISSN: 0037-1017

  56. 線虫VIP36 orthologue-ILE-2の機能解析

    福島 慶子, 井手尾 浩子, 安藤 恵子, 三谷 昌平, 出嶋 克史, 野村 一也, 山下 克子

    日本生化学会大会プログラム・講演要旨集 82回 3T10p-11 2009/09

    Publisher: (公社)日本生化学会

    ISSN: 0037-1017

  57. グリセロ脂質 de novo 合成に関与する脂肪酸転移酵素の包括的解析

    櫻木 健司, 井上 貴雄, 原 直子, 河野 望, 安藤 恵子, 三谷 昌平, 新井 洋由

    脂質生化学研究 51 43-46 2009/07/10

    ISSN: 0285-1520

  58. メンブレントラフィクに関与する線虫Sec1/Munc18ファミリーのゲノム機能解析(Functional genomics analysis of the C. elegans Sec1/Munc18 family involved in membrane traffic)

    安藤 恵子, 中臺 枝里子, 三谷 昌平

    日本細胞生物学会大会講演要旨集 61回 204-204 2009/05

    Publisher: (一社)日本細胞生物学会

  59. 線虫C.elegansを用いた高度不飽和度脂肪酸欠乏下における小胞体ストレス応答の活性化機構の解析

    田中 陸人, 平田 祐介, 河野 望, 井上 貴雄, 鈴木 健裕, 堂前 直, 安藤 恵子, 三谷 昌平, 新井 洋由

    日本薬学会年会要旨集 129年会 (3) 104-104 2009/03

    Publisher: (公社)日本薬学会

    ISSN: 0918-9823

  60. 線虫を用いたSNARE分子GS28の機能解析

    前川 大志, 井上 貴雄, 小鮒 弘幸, 西村 多喜, 安藤 恵子, 三谷 昌平, 新井 洋由

    日本薬学会年会要旨集 129年会 (3) 132-132 2009/03

    Publisher: (公社)日本薬学会

    ISSN: 0918-9823

  61. 線虫を用いたヒト遺伝子のオーソログ分子の機能解析

    三谷昌平, 藤澤和子, 安藤恵子, 茂泉佐和子, 鴻宗義, 中台枝里子, 榊建二郎, 林亜紀, 小鮒弘幸

    東京女子医科大学総合研究所紀要 29 2009

    ISSN: 0911-4491

  62. 線虫におけるセラミドグルコシル転移酵素の機能解明

    野村和子, 村田大輔, 村田大輔, 宮崎清香, 出嶋克史, 出嶋克史, 水口惣平, 水口惣平, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 林康宏, 林康宏, 伊東信, 伊東信, 平林義雄, 平林義雄, 野村一也, 野村一也

    日本分子生物学会年会講演要旨集 32nd (Vol.1) 2009

  63. “代謝調節機構解析に基づく細胞機能制御基盤技術”研究領域 極長鎖アシルCoAシンテターゼの表皮バリアーにおける役割の解析-線虫C.elegansを用いた機能解析-

    中台(鹿毛)枝里子, 小鮒弘幸, 木村真子, 安藤恵子, 井上貴雄, 新井洋由, 三谷昌平

    代謝調節機構解析に基づく細胞機能制御基盤技術研究領域 第2回公開シンポジウム講演要旨集 平成21年 2009

  64. The Arf-like GTPase ARL-8 is required for lysosome biogenesis in C. elegans

    中江郁青, 佐々木文佳, 安藤恵子, 三谷昌平, 紺谷圏二, 堅田利明

    日本分子生物学会年会講演要旨集 32nd (Vol.3) 2009

  65. GPIアンカー生合成遺伝子機能阻害による線虫C.elegans生殖系列の表現型解析

    村田大輔, 村田大輔, 野村和子, 野村和子, 水口惣平, 水口惣平, 出嶋克史, 出嶋克史, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 福島慶子, 福島慶子, 山下克子, 山下克子, 中島紫, 中島紫, 伊藤さつき, 川崎ナナ, 川崎ナナ, 野村一也, 野村一也

    日本分子生物学会年会講演要旨集 32nd (Vol.1) 2009

  66. 線虫における硫酸化関連遺伝子の遺伝子ノックアウト

    野村一也, 出嶋克史, 水口惣平, 村田大輔, 野村和子, 安藤恵子, 三谷昌平, 瀬古玲, 山下克子, 泉川友美, 菅原一幸, 北川裕之

    日本糖質学会年会要旨集 29th 2009

  67. SYSTEMATIC ISOLATION OF MUTANTS DEFECTIVE IN TRANSCRIPTION FACTORS IN C. ELEGANS

    Shohei Mitani, Keiko Gengyo-Ando, Sawako Yoshina, Eriko Kage-Nakadai, Muneyoshi Otori, Kenjiro Sakaki, Kazuko Fujisawa, Hiroyuki Kobuna

    JOURNAL OF PHYSIOLOGICAL SCIENCES 59 43-43 2009

    ISSN: 1880-6546

  68. リン脂質生合成系に関与する脂肪酸転移酵素の系統的解析

    櫻木健司, 井上貴雄, 原直子, 今江理恵子, 河野望, 鴻宗義, 安藤恵子, 三谷昌平, 新井洋由

    衛生薬学・環境トキシコロジー講演要旨集 2008 101 2008/10/03

    ISSN: 0919-2115

  69. 線虫C. elegansにおけるMBOATファミリーの機能解析

    松田 真治, 井上 貴雄, 李 賢哲, 河野 望, 田中 史晴, 安藤 恵子, 三谷 昌平, 新井 洋由

    脂質生化学研究 50 180-183 2008/05

    Publisher: 日本脂質生化学会

    ISSN: 0285-1520

  70. 線虫C.elegansを用いた高度不飽和脂肪酸依存的な転写制御機構の解明

    平田 祐介, 河野 望, 井上 貴雄, 鈴木 健裕, 堂前 直, 安藤 恵子, 三谷 昌平, 新井 洋由

    脂質生化学研究 50 204-207 2008/05

    Publisher: 日本脂質生化学会

    ISSN: 0285-1520

  71. C.elegansを用いた硫酸化修飾関連遺伝子の器官形成における役割と硫酸供与体PAPSの合成・輸送機構の解析

    出嶋克史, 出嶋克史, 瀬古玲, 瀬古玲, 山下克子, 山下克子, 泉川友美, 泉川友美, 北川裕之, 北川裕之, 菅原一幸, 菅原一幸, 野村和子, 野村和子, 水口惣平, 水口惣平, 村田大輔, 村田大輔, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 野村一也, 野村一也, 野村一也

    生化学 2008

    ISSN: 0037-1017

  72. 線虫におけるセラミドグルコシル転移酵素の機能解明

    野村和子, 野村和子, 村田大輔, 村田大輔, 水口惣平, 水口惣平, 出嶋克史, 出嶋克史, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 林康広, 林康広, 伊東信, 伊東信, 平林義雄, 平林義雄, 野村一也, 野村一也

    生化学 2008

    ISSN: 0037-1017

  73. マニュアル変更が及ぼす中心静脈カテーテル関連血流感染のサーベイランス報告

    岩本里美, 安藤恵子, 高山保子, 川合悦子, 松井三紀, 西口貴恵, 河合浩樹, 原田正弥, 三宅孝

    環境感染 23 (Supplement) 2008

    ISSN: 0918-3337

  74. 代謝調節機構解析に基づく細胞機能制御基盤技術 生体膜リン脂質多様性の構築機構の解明と高度不飽和脂肪酸要求性蛋白質の同定

    新井洋由, 安藤恵子

    代謝調節機構解析に基づく細胞機能制御基盤技術研究領域 第1回公開シンポジウム講演要旨集 平成20年 2008

  75. 線虫C.elegansを用いたGS28(Golgi SNARE of 28kDa)の機能解析

    前川大志, 井上貴雄, 井上貴雄, 小鮒弘幸, 西村多喜, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 新井洋由, 新井洋由

    衛生薬学・環境トキシコロジー講演要旨集 2008 2008

    ISSN: 0919-2115

  76. GPIアンカー生合成遺伝子機能阻害における線虫Caenorhabditis elegansの表現型解析

    村田大輔, 村田大輔, 野村和子, 野村和子, 水口惣平, 水口惣平, 出嶋克史, 出嶋克史, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 福島慶子, 福島慶子, 山下克子, 山下克子, 中島紫, 中島紫, 伊藤さつき, 川崎ナナ, 川崎ナナ, 野村一也, 野村一也

    生化学 2008

    ISSN: 0037-1017

  77. モデル生物C.elegansを用いたコンドロイチンプロテオグリカンの生体内機能解析

    水口惣平, 水口惣平, 野村和子, 野村和子, 出嶋克史, 出嶋克史, 泉川友美, 泉川友美, 中島紫, 中島紫, 伊藤さつき, 川崎ナナ, 川崎ナナ, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 北川裕之, 北川裕之, 菅原一幸, 野村一也, 野村一也

    生化学 2008

    ISSN: 0037-1017

  78. Identification and expression analysis of upd (upregulated proteins under PUFA-depleted conditions) genes in C. elegans

    田中陸人, 平田祐介, 河野望, 河野望, 井上貴雄, 井上貴雄, 鈴木健裕, 堂前直, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 新井洋由, 新井洋由

    生化学 2008

    ISSN: 0037-1017

  79. 線虫C.elegansを用いた高度不飽和脂肪酸依存的な遺伝子発現誘導機構の解析

    平田祐介, 田中陸人, 河野望, 河野望, 井上貴雄, 井上貴雄, 有山博之, 鈴木健裕, 堂前直, 安藤恵子, 安藤恵子, 三谷昌平, 新井洋由, 新井洋由

    生化学 2008

    ISSN: 0037-1017

  80. Functional analysis of acl‐10, an evolutionarily conserved acyltransferase in C. elegans

    今江理恵子, 井上貴雄, 原直子, 安藤恵子, 三谷昌平, 新井洋由

    生化学 2P-0045 2008

    ISSN: 0037-1017

  81. Systematic analysis of acyltransferases involved in de novo glycerophospholipid synthesis using C.elegans mutants

    櫻木健司, 井上貴雄, 原直子, 今江理恵子, 河野望, 鴻宗義, 安藤恵子, 三谷昌平, 新井洋由

    生化学 2P-0044 2008

    ISSN: 0037-1017

  82. Functional genomics on the Sec1/Munc18 family in membrane trafficking of C. elegans

    Keiko Gengyo-Ando, Shoheni Mitani

    GENES & GENETIC SYSTEMS 82 (6) 502-502 2007/12

    ISSN: 1341-7568

    eISSN: 1880-5779

  83. リソソームにおけるArf様small GTPase Arl8の機能的解析(Functional analysis of the Arf-like small GTPase Arl8 in lysosomes)

    紺谷 圏二, 藤野 知子, 小林 哲夫, 中江 郁青, 菊香 順史, 原田 さやか, 安藤 恵子, 三谷 昌平, 堅田 利明

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集 80回・30回 3S15-4 2007/11

    Publisher: (公社)日本生化学会

  84. 線虫C.elegansを用いた高度不飽和脂肪酸感受性遺伝子の探索

    白江伸一郎, 井上貴雄, 原直子, 安藤恵子, 三谷昌平, 新井洋由

    衛生薬学・環境トキシコロジー講演要旨集 2007 116 2007/10/10

    ISSN: 0919-2115

  85. オキシステロール結合蛋白質ファミリー(ORPファミリー)の機能解析

    井上 貴雄, 小鮒 弘幸, 芝田 真知子, 安藤 恵子, 三谷 昌平, 新井 洋由

    脂質生化学研究 49 77-79 2007/05

    Publisher: 日本脂質生化学会

    ISSN: 0285-1520

  86. ERストレス応答におけるC.elegansメタロプロテアーゼの機能的解析(Functional analysis of C. elegans metalloprotease in ER stress response)

    吉名 佐和子, 安藤 恵子, 飯野 雄一, 井上 英史, 三谷 昌平

    日本発生生物学会・日本細胞生物学会合同大会要旨集 40回・59回 76-76 2007/05

    Publisher: 日本発生生物学会・日本細胞生物学会

  87. Caenorhabditis elegansのRAB-5依存性エンドサイトーシス輸送におけるSec1/Munc18タンパク質の生理学的役割(Physiological role of the Sec1/Munc18 protein VPS-45 in the RAB-5-dependent endocytic trafficking in Caenorhabditis elegans)

    安藤 恵子, 黒柳 秀人, 小林 哲夫, 村手 源英, 藤本 和, 岡部 繁男, 三谷 昌平

    日本発生生物学会・日本細胞生物学会合同大会要旨集 40回・59回 195-195 2007/05

    Publisher: 日本発生生物学会・日本細胞生物学会

  88. 線虫におけるセラミドグルコシル転移酵素の機能解明

    野村和子, 野村和子, 林康宏, 林康宏, 村田大輔, 村田大輔, 永石貴之, 永石貴之, 水口惣平, 水口惣平, 出嶋克史, 出嶋克史, 福嶋宏史, 福嶋宏史, 中島紫, 中島紫, 川崎ナナ, 川崎ナナ, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 伊東信, 伊東信, 平林義雄, 平林義雄, 野村一也, 野村一也

    日本糖質学会年会要旨集 27th 2007

  89. In vivo incorporation of radiolabeled fatty acids into C. elegans

    松田真治, 井上貴雄, 井上貴雄, 今江理恵子, 櫻木健司, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 新井洋由, 新井洋由

    生化学 2007

    ISSN: 0037-1017

  90. モデル生物C.elegansを用いたヘパラン硫酸の生体内機能解析

    水口惣平, 水口惣平, 野村和子, 野村和子, 出嶋克史, 出嶋克史, 泉川友美, 泉川友美, 江草徳幸, 谷口史恭, 田村純一, 安藤恵子, 安藤恵子, 三谷昌平, 北川裕之, 北川裕之, 菅原一幸, 菅原一幸, 野村一也, 野村一也

    日本糖質学会年会要旨集 27th 2007

  91. 線虫C.elegansを用いた硫酸化修飾関連遺伝子の発生過程における役割と硫酸供与体PAPSの合成制御機構の解析

    出嶋克史, 出嶋克史, 瀬古玲, 瀬古玲, 山下克子, 山下克子, 泉川友美, 泉川友美, 北川裕之, 北川裕之, 菅原一幸, 菅原一幸, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 水口惣平, 水口惣平, 野村和子, 野村和子, 村田大輔, 村田大輔, 野村一也, 野村一也

    生化学 2007

    ISSN: 0037-1017

  92. 線虫におけるセラミドグルコシル転移酵素の機能解明

    野村和子, 林康広, 林康広, 村田大輔, 村田大輔, 永石貴之, 永石貴之, 水口惣平, 水口惣平, 出嶋克史, 出嶋克史, 福嶋宏史, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 中島紫, 中島紫, 川崎ナナ, 川崎ナナ, 伊東信, 伊東信, 平林義雄, 平林義雄, 野村一也, 野村一也

    生化学 2007

    ISSN: 0037-1017

  93. 線虫C.elegansのABC輸送体haf-2の発現解析

    脇本菜有, 大橋綾子, 大橋綾子, 安藤恵子, 三谷昌平, 前田正知

    生化学 2007

    ISSN: 0037-1017

  94. 繊毛における低分子量Gタンパク質Arl-13bの機能解析

    小林哲夫, 堀裕次, 安藤恵子, 三谷昌平, 紺谷圏二, 堅田利明

    生化学 2007

    ISSN: 0037-1017

  95. 線虫を用いた低分子G蛋白質Arl8のリソソームにおける機能解析

    藤野知子, 小林哲夫, 中江郁青, 安藤恵子, 三谷昌平, 紺谷圏二, 堅田利明

    生化学 2007

    ISSN: 0037-1017

  96. 線虫C.elegansにおけるGPIアンカーの機能解析

    村田大輔, 村田大輔, 野村和子, 野村和子, 水口惣平, 水口惣平, 出嶋克史, 出嶋克史, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 福島慶子, 福島慶子, 山下克子, 山下克子, 中島紫, 中島紫, 伊藤さつき, 川崎ナナ, 川崎ナナ, 野村一也, 野村一也

    生化学 2007

    ISSN: 0037-1017

  97. モデル生物C.elegansを用いたヘパラン硫酸とコンドロイチンプロテオグリカンの生体内機能解析

    水口惣平, 水口惣平, 野村和子, 野村和子, 出嶋克史, 出嶋克史, 泉川友美, 泉川友美, 江草徳幸, 谷口史恭, 田村純一, 中島紫, 中島紫, 伊藤さつき, 川崎ナナ, 川崎ナナ, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 北川裕之, 北川裕之, 菅原一幸, 菅原一幸, 野村一也, 野村一也

    生化学 2007

    ISSN: 0037-1017

  98. Homolog of UDP-gal transporter(HUT-1)は線虫Caenorhabditis elegansにおいて小胞体機能と幼虫発生に必須である。

    出嶋克史, 出嶋克史, 水口惣平, 水口惣平, 野村和子, 野村和子, 村田大輔, 村田大輔, 平田拓, 平田拓, 金井好克, 金井好克, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 野村一也, 野村一也

    日本糖質学会年会要旨集 27th 2007

  99. 線虫C.elegansにおけるGPIアンカーの機能解析

    村田大輔, 村田大輔, 野村和子, 野村和子, 水口惣平, 水口惣平, 出嶋克史, 出嶋克史, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 福島慶子, 福島慶子, 山下克子, 山下克子, 野村一也, 野村一也

    日本糖質学会年会要旨集 27th 2007

  100. Rasファミリー蛋白質DRN-1の線虫神経系における機能解析

    多田稔, 小林哲夫, 安藤恵子, 三谷昌平, 紺谷圏二, 堅田利明

    生化学 2007

    ISSN: 0037-1017

  101. 哺乳動物ガレクチン-4様線虫ガレクチンの機能解析

    井手尾浩子, 井手尾浩子, 福島慶子, 福島慶子, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 出嶋克史, 出嶋克史, 野村一也, 野村一也, 山下克子, 山下克子

    日本糖質学会年会要旨集 27th 2007

  102. 線虫C.elegansのprotein phsophatase2Aとオートファジー関連キナーゼUNC-51/Atg1は,協調して軸索ガイダンスを制御している。

    小倉顕一, 三谷昌平, 安藤恵子, BAILLIE David, 小原雄治, 五嶋良郎, 五嶋良郎

    生化学 2007

    ISSN: 0037-1017

  103. 線虫C.elegansを用いた高度不飽和脂肪酸(PUFA)要求性遺伝子の探索

    白江伸一郎, 井上貴雄, 原直子, 安藤恵子, 三谷昌平, 新井洋由

    生化学 2P-0131 2007

    ISSN: 0037-1017

  104. 線虫におけるグリコサミノグリカン鎖の生合成機構とその機能

    泉川友美, 泉川友美, 水口惣平, 水口惣平, 江草徳幸, 谷口史恭, 出島克史, 出島克史, 野村和子, 野村和子, 田村純一, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 野村一也, 野村一也, 菅原一幸, 菅原一幸, 菅原一幸, 北川裕之, 北川裕之

    日本糖質学会年会要旨集 26th 2006

  105. 遺伝子破壊による線虫糖鎖関連遺伝子の機能解析

    野村一也, 野村一也, 水口惣平, 水口惣平, 野村和子, 野村和子, 出嶋克史, 出嶋克史, 永石貴之, 永石貴之, 村田大輔, 村田大輔, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 瀬古玲, 瀬古玲, 山下克子, 山下克子, 泉川友美, 泉川友美, 北川裕之, 北川裕之, 菅原一幸, 菅原一幸, 川崎ナナ, 川崎ナナ, 中島紫, 中島紫, KWON Yeon-Dae, 成松久

    日本糖質学会年会要旨集 26th 2006

  106. 線虫を用いた機能分子の系統的欠失変異体分離と機能解析

    三谷 昌平, 安藤 恵子

    東京女子医科大学総合研究所紀要 25 20-20 2005/07

    Publisher: 東京女子医科大学総合研究所

    ISSN: 0911-4491

  107. C.elegansのDistal Tip Cellの移動に関与するプロテアーゼ群

    吉名佐和子, 安藤恵子, 三谷昌平, 飯野雄一, 柳茂, 高橋健治, 井上英史

    日本分子生物学会年会講演要旨集 28th 2005

  108. C.elegansのコンドロイチン生合成および初期はいにおける細胞質分裂に必須であるコンドロイチン重合化因子(cChPF;PAR2.4)の同定

    泉川友美, 北川裕之, 水口惣平, 野村和子, 野村一也, 田村純一, 安藤恵子, 三谷昌平, 菅原一幸

    日本薬学会年会要旨集 125th (3) 2005

    ISSN: 0918-9823

  109. 線虫C.elegans分泌型セマフォリン,プレキシン,エフリンの表皮形態形成における働き

    鈴木基史, 中尾史, 劉致しん, 黒河理絵, 糠塚明, 安藤恵子, 三谷昌平, 藤沢肇, 高木新

    日本発生生物学会大会発表要旨集 38th 2005

  110. 遺伝子破壊による糖鎖機能の戦略的解明-線虫 C.elegans を用いた解析の中間報告

    水口惣平, 水口惣平, 野村和子, 野村和子, 出嶋克史, 出嶋克史, 永石貴之, 三谷昌平, 安藤恵子, 安藤恵子, 川崎ナナ, 川崎ナナ, 松石ゆかり, 松石ゆかり, 橋井則貴, 橋井則貴, 瀬古玲, 瀬古玲, 山下克子, 泉川友美, 泉川友美, 北川裕之, 北川裕之, 菅原一幸, 菅原一幸, 平林義雄, 平林義雄, KWON Yeon-Dae, 成松久, 野村一也, 野村一也

    日本分子生物学会年会講演要旨集 28th 2005

  111. 線虫 C.elegans を用いた複合糖質硫酸化修飾に関連した遺伝子の解析

    出嶋克史, 出嶋克史, 野村和子, 野村和子, 水口惣平, 水口惣平, 安藤恵子, 安藤恵子, 三谷昌平, 瀬古玲, 瀬古玲, 山下克子, 平林義雄, 野村一也, 野村一也

    日本分子生物学会年会講演要旨集 28th 2005

  112. C.elegansの糖鎖付加タンパク質の決定

    永石貴之, 野村和子, 野村和子, 水口惣平, 水口惣平, 出嶋克史, 出嶋克史, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 平林義雄, 松石ゆかり, 橋井則貴, 川崎ナナ, 野村一也, 野村一也

    日本分子生物学会年会講演要旨集 28th 2005

  113. 線虫vps-45および相互作用するsyntaxin遺伝子の逆遺伝学的解析

    安藤恵子, 安藤恵子, 小林哲夫, 小林哲夫, 瀬山陽一, 瀬山陽一, 三谷昌平

    日本分子生物学会年会講演要旨集 28th 2005

  114. 線虫におけるGタンパク質制御因子AGS-3の機能解析

    小林哲夫, 小林哲夫, 安藤恵子, 安藤恵子, 石原健, 石原健, 桂勲, 三谷昌平

    日本分子生物学会年会講演要旨集 28th 2005

  115. 線虫 C.elegans における高浸透圧ストレスや酸化ストレスに対する応答にクチクラ層の構成成分OSM-7が関与する

    間瀬慶子, 小野寺章, 梁瀬澄乃, 安藤恵子, 三谷昌平, 大島靖美, 桂勲, 石井直明, 石原健, 古賀誠人

    日本分子生物学会年会講演要旨集 28th 2005

  116. C.elegansを用いた糖鎖の網羅的機能解析 二次元電気泳動(2D-DIGE)によるアセチル化の定量的解析

    野村和子, 野村和子, 水口惣平, 水口惣平, 出嶋克史, 出嶋克史, 永石貴之, 安藤恵子, 安藤恵子, 三谷昌平, 三谷昌平, 平林義雄, 松石ゆかり, 橋井則貴, 川崎ナナ, 野村一也, 野村一也

    日本分子生物学会年会講演要旨集 28th 2005

  117. Systematic proteome analysis of glycome-related genes in the nematode C.elegans

    野村和子, 野村和子, 水口惣平, 水口惣平, 永石貴之, 永石貴之, 安藤恵子, 安藤恵子, 三谷昌平, 平林義雄, 松石紫, 川崎ナナ, 野村一也, 野村一也

    日本プロテオーム学会大会プログラム・抄録集 2005 (Web) 2005

  118. ミトコンドリアATP合成酵素bサブユニットの生殖系列特異的なアイソフォーム

    川崎一郎, 花沢桃世, 花沢桃世, 安藤恵子, 三谷昌平, 飯野雄一

    日本分子生物学会年会講演要旨集 28th 2005

  119. タウオパチーの線虫モデル(C.elegans model of tauopathy)

    丁 震, 宮坂 知宏, 安藤 恵子, 三谷 昌平, 井原 康夫

    神経化学 43 (2-3) 371-371 2004/08

    Publisher: 日本神経化学会

    ISSN: 0037-3796

  120. メンブレントラフィックに関わる線虫Sec1/Munc-18ファミリー遺伝子Ce-vps45の機能解析(Functional analysis of the C.elegans Sec1/Munc-18 family gene Ce-vps45 involved in membrane traffic)

    安藤 恵子, 町山 悦子, 野口 幸子, 三谷 昌平

    神経化学 43 (2-3) 470-470 2004/08

    Publisher: 日本神経化学会

    ISSN: 0037-3796

  121. [Chondroitin sugars in embryonic cell division of the nematode C. elegans].

    Souhei Mizuguchi, Kazuko H Nomura, Katsufumi Dejima, Kazuya Nomura, Kazuyuki Sugahara, Hiroshi Kitagawa, Toru Uyama, Shohei Mitani, Keiko Gengyo-Ando

    Tanpakushitsu kakusan koso. Protein, nucleic acid, enzyme 49 (2) 141-7 2004/02

    ISSN: 0039-9450

  122. 線虫の細胞分裂を制御する糖鎖コンドロイチン

    水口 惣平, 野村 和子, 出嶋 克史, 安藤 恵子, 三谷 昌平, 宇山 徹, 北川 裕之, 菅原 一幸, 野村 一也

    蛋白質・核酸・酵素 49 (2) 141-147 2004/02

    Publisher: 共立出版(株)

    ISSN: 0039-9450

  123. 線虫Caenorhabditis.elegansを用いた複合糖質硫酸化修飾に関連した遺伝子の解析

    出嶋克史, 野村和子, 水口惣平, 安藤恵子, 三谷昌平, 瀬古玲, 山下克子, 平林義雄, 野村一也

    日本分子生物学会年会プログラム・講演要旨集 27th 2004

  124. ジペプチジルペプチダーゼIV様プロテアーゼはC.elegansの遠端細胞移動の調節に必須である(原標題は英語)

    吉名佐和子, 安藤恵子, 三谷昌平, 飯野雄一, 井上英史, 高橋健治

    日本分子生物学会年会プログラム・講演要旨集 27th 2004

  125. 二次元電気泳動を用いた線虫Acetyl CoAトランスポーターの解析

    野村和子, 水口惣平, 安藤恵子, 三谷昌平, 平林義雄, 松石紫, 川崎ナナ, 出嶋克史, 野村一也

    日本分子生物学会年会プログラム・講演要旨集 27th 2004

  126. 細胞分裂と形態形成を支配する糖鎖-モデル生物Caenorhabditis elegansを用いた機能解析

    水口惣平, 野村和子, 安藤恵子, 三谷昌平, 川崎ナナ, 金井好克, 瀬古玲, 北川裕之, 菅原一幸

    日本分子生物学会年会プログラム・講演要旨集 27th 2004

  127. ドパミンニューロン特異的にα-シヌクレインを発現するトランスジェニック線虫の作出と解析

    桑原 知樹, 小山 彰比古, 安藤 恵子, 三谷 昌平, 岩坪 威

    Dementia Japan 17 (2) 178-178 2003/08

    Publisher: (一社)日本認知症学会

    ISSN: 1342-646X

  128. 線虫を用いた機能分子の系統的欠失変異体分離と機能解析

    三谷 昌平, 安藤 恵子

    東京女子医科大学総合研究所紀要 23 18-18 2003/07

    Publisher: 東京女子医科大学総合研究所

    ISSN: 0911-4491

  129. ナショナルバイオリソースプロジェクト「実験動物・線虫」

    三谷昌平, 安藤恵子

    日本分子生物学会年会プログラム・講演要旨集 26th 2003

  130. 転写因子遺伝子群の体系的遺伝子破壊による 線虫 C.elegans のゲノム機能解析

    安藤恵子, 三谷昌平

    日本分子生物学会年会プログラム・講演要旨集 26th 2003

  131. Caenorhabditis elegans初期はい細胞質分裂に関与するコンドロイチンプロテオグリカンの解析

    水口惣平, 宇山徹, 北川裕之, 野村和子, 出嶋克史, 安藤恵子, 三谷昌平, 菅原一幸, 野村一也

    日本分子生物学会年会プログラム・講演要旨集 26th 2003

  132. 線虫Acetyl CoA transporter遺伝子の発現解析

    野村和子, 水口惣平, 安藤恵子, 三谷昌平, 平林義雄, 野村一也

    日本分子生物学会年会プログラム・講演要旨集 26th 2003

  133. インスリン様遺伝子破壊線虫の解析

    河野強, 石井良子, 木村靖夫, 安藤恵子, 三谷昌平

    日本分子生物学会年会プログラム・講演要旨集 26th 2003

  134. ポストゲノム研究のミッシング・リンク-糖鎖シグナルによる生体機能調節 線虫グリコーム関連遺伝子のRNAiによる解析-中間報告

    野村 一也, 水口 惣平, 野村 和子, 出嶋 克史, 宇山 徹, 北川 裕之, 菅原 一幸, 三谷 昌平, 安藤 恵子, 小原 雄治, 平林 義雄

    生化学 74 (8) 648-648 2002/08

    Publisher: (公社)日本生化学会

    ISSN: 0037-1017

  135. 細胞分化と分裂を制御する糖鎖の解析

    水口 惣平, 野村 和子, 出嶋 克史, 菅原 一幸, 北川 裕之, 宇山 徹, 三谷 昌平, 安藤 恵子, 小原 雄治, 平林 義雄, 野村 一也, Schmid Volker

    生化学 74 (8) 803-803 2002/08

    Publisher: (公社)日本生化学会

    ISSN: 0037-1017

  136. ゴルジ体から液胞/リソソームへの輸送経路に関与する線虫vps45ホモログ(Cevps45)の機能解析

    安藤 恵子, 町山 悦子, 野口 幸子, 三谷 昌平

    神経化学 40 (2-3) 336-336 2001/09

    Publisher: 日本神経化学会

    ISSN: 0037-3796

  137. 線虫を用いた転写制御因子を中心とした機能分子の系統的欠失変異体分離

    三谷 昌平, 安藤 恵子, 町山 悦子, 野口 幸子

    東京女子医科大学総合研究所紀要 21 20-20 2001/07

    Publisher: 東京女子医科大学総合研究所

    ISSN: 0911-4491

  138. ゴルジ体から液胞/リソソームへの輸送経路に関与する線虫vps45ホモログ(Cevps45)の機能解析

    安藤恵子, 町山悦子, 野口幸子, 三谷昌平

    日本神経科学大会プログラム・抄録集 24th 2001

    ISSN: 1347-8583

  139. 線虫C.elegansを使って糖鎖の機能を探る Acetyl CoA transporterを例として

    野村一也, 水口惣平, 野村和子, 三谷昌平, 安藤恵子, 平林義雄

    日本糖質学会年会要旨集 22nd 2001

  140. Functional ayalysis of protein phosphatase 1 in C.elegans.

    佐々寿浩, 北村敬一郎, 原田真市, 平野佳奈子, 安藤恵子, 三谷昌平, 細野隆次

    生体分子科学討論会講演要旨集 28th 2001

  141. モデル生物を使ったゲノムシーケンス決定後の分子遺伝学

    三谷 昌平, 安藤 恵子, 米積 亜紀, 町山 悦子, 阪本 照美, 野口 幸子

    東京女子医科大学雑誌 70 (9) 612-613 2000/09

    Publisher: 東京女子医科大学学会

    ISSN: 0040-9022

  142. 【顕微鏡フル活用術イラストレイテッド 基礎から応用まで】 生体を観察・記録する 線虫

    三谷 昌平, 安藤 恵子

    細胞工学 別冊 (顕微鏡フル活用術イラストレイテッド) 105-108 2000/07

    Publisher: (株)学研メディカル秀潤社

    ISSN: 0287-3796

  143. 遺伝子破壊による線虫転写因子遺伝子群の網羅的逆遺伝学的解析

    安藤恵子, 町山悦子, 野口幸子, 三谷昌平

    日本分子生物学会年会プログラム・講演要旨集 23rd 2000

  144. Functional analysis of protein phosphatase 1(pp1-1) in C.elegans

    佐々寿浩, XU X, 上田寛子, 安藤恵子, 三谷昌平, 北村敬一郎, 細野隆次

    日本分子生物学会年会プログラム・講演要旨集 23rd 2000

  145. 線虫を用いた糖鎖の系統的機能解析

    野村一也, 野村和子, 水口惣平, 高木哲郎, 三谷昌平, 安藤恵子, 平林義雄

    日本分子生物学会年会プログラム・講演要旨集 23rd 2000

  146. 伝達物質放出に関与する線虫Sec1ファミリー遺伝子C44C1.4の発現と機能解析

    安藤恵子, 三谷昌平

    日本神経科学大会プログラム・抄録集 23rd 2000

    ISSN: 1347-8583

  147. 線虫を用いた系統的欠失変異体分離のための凍結保存変異体バンクの作製とパイロットスクリーニング

    三谷昌平, 安藤恵子, 町田悦子, 野口幸子

    東京女子医科大学総合研究所紀要 20 1999

    ISSN: 0911-4491

  148. 開口放出に関与する線虫UNC-18ファミリーB0303.9の構造と発現解析

    安藤恵子, 三谷昌平

    日本分子生物学会年会プログラム・講演要旨集 22nd 1999

  149. 開口放出に関与する線虫UNC-18ファミリーの構造と発現解析

    安藤恵子, 三谷昌平

    日本神経科学大会プログラム・抄録集 22nd 1999

    ISSN: 1347-8583

  150. 線虫を用いた大規模逆遺伝学のための欠失変異体分離法の開発 (文部省S)

    三谷昌平, 安藤恵子

    ゲノムサイエンス:ヒトゲノム解析に基づくバイオサイエンスの新展開 平成10年度 No.08283101 1999

  151. Efficient isolation of deletion mutants for reverse genetics in C. elegans

    GENGYO-ANDO Keiko, MITANI Shohei

    21 334-334 1998/12/01

  152. 逆遺伝学的解析法のための線虫C.elegans遺伝子破壊法の効率化

    安藤 恵子, 三谷 昌平

    神経化学 37 (3) 322-322 1998/09

    Publisher: 日本神経化学会

    ISSN: 0037-3796

  153. Efficient isolation of deletion mutants by trimethylpsoralen and UV.

    三谷昌平, 安藤恵子

    東京女子医科大学総合研究所紀要 19 1998

    ISSN: 0911-4491

  154. Nematode C.elegans in life science.

    安藤恵子

    Medical Technology 25 (6) 1997

    ISSN: 0389-1887

  155. Identification of the Target Genes for POU Domain Transcription Factor UNC-86 Using Epitope-Tagging in the Nematode C.elegans.

    安藤恵子, 三谷昌平

    日本分子生物学会年会プログラム・講演要旨集 20th 1997

  156. デジタル画像解析を用いたC.elegans unc-18突然変異体における神経伝達物質蓄積の検討

    安藤 恵子

    生化学 68 (7) 714-714 1996/07

    Publisher: (公社)日本生化学会

    ISSN: 0037-1017

  157. シナプス伝達障害による異常行動の基礎的研究

    安藤 恵子

    日本法医学雑誌 50 (補冊) 212-212 1996/04

    Publisher: (NPO)日本法医学会

    ISSN: 0047-1887

  158. 神経伝達物質の動態制御に関与するunc-18遺伝子ファミリーの分子生物学的研究

    安藤 恵子

    防衛医科大学校雑誌 21 (1) 65-65 1996/03

    Publisher: 防衛医科大学校雑誌編集委員会

    ISSN: 0385-1796

  159. Structure and function of mouse homologue of C. elegans unc-18 gene involved in neurotransmitter release.

    安藤恵子, 北山仁志, 井川洋二

    日本分子生物学会年会プログラム・講演要旨集 17th 1994

  160. Mouse unc-18 homologous genes participating in the neurotransmitter release.

    安藤恵子, 北山仁志, 井川洋二

    日本細胞生物学会大会講演要旨集 47th 1994

  161. シナプス伝達の分子機構

    細野隆次, 安藤恵子, 井川洋二, 原田真市, 山本博, 小川久光

    日本分子生物学会年会プログラム・講演要旨集 16th 1993

  162. 線虫の筋発生における組織特異的遺伝子発現と分子集合

    安藤 恵子, 香川 弘昭

    細胞工学 10 (9) 687-694 1991/09

    Publisher: (株)学研メディカル秀潤社

    ISSN: 0287-3796

  163. Antigenic sites of the muscle protein, paramyosin, in Caenorhabditis elegans determined with exon-expression plasmid. International-journal

    H Kagawa, K Gengyo

    Nucleic acids symposium series (19) 81-4 1988

    ISSN: 0261-3166

    More details Close

    Sonicated and restricted DNA fragments from plasmid clones containing the paramyosin gene, unc-15 in C. elegans were recloned into lac-z expression plasmid vectors. Numerous fragments were recovered which encoded paramyosin epitopes. These clones produced fusion protein which cross-reacted with a polyclonal and three monoclonal antibodies. The samples of sonicated fragments were also used for shot gun sequencing of the gene. Sequenced fragments were aligned with a computer analysis. Amino acid sequence of the expressed clones matched exactly to that of the exon.

  164. HOMOLOGY BETWEEN UNC-15, PARAMYOSIN GENE AND UNC-54, MYOSIN HEAVY-CHAIN GENE OF CHAENORHABDITIS-ELEGANS

    H KAGAWA, K GENGYO

    JAPANESE JOURNAL OF GENETICS 62 (6) 524-524 1987/12

    ISSN: 0021-504X

  165. GENE STRUCTURE OF THE PARAMYOSIN GENE, UNC-15 OF CAENORHABDITIS ELEGANS

    H KAGAWA, K GENGYO, M NOJI

    JAPANESE JOURNAL OF GENETICS 61 (6) 587-588 1986/12

    ISSN: 0021-504X

Show all ︎Show first 5

Presentations 2

  1. in vivo calcium imaging, membrane trafficking and taste preference Invited

    Junichi Nakai, Keiko Gengyo-Ando, Tadaaki Kudo

    2022 8th International Conference on Mechatronics and Robotics Engineering (ICMRE) 2022/12/15

  2. Membrane trafficking Invited

    Keiko Gengyo-Ando

    21th Yonsei Dental International Symposium 2022/06/27

Industrial Property Rights 2

  1. 線虫を用いた物質の生理活性評価法

    中井 淳一, 安藤 恵子

    特許第7045680号

    Property Type: Patent

  2. 線虫を用いた物質の生理活性評価法

    中井 淳一, 安藤 恵子

    Property Type: Patent

Research Projects 25

  1. エンドソームの機能異常による疾患メカニズムの研究

    安藤 恵子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(C)

    Institution: 東北大学

    2025/04/01 - 2028/03/31

  2. Development of X-logbot and Elucidation of Behavior Diagram using Sparse Modeling

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Transformative Research Areas (A)

    Category: Grant-in-Aid for Transformative Research Areas (A)

    Institution: Tohoku University

    2021/09/10 - 2026/03/31

  3. A novel animal model of sarcopenia

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Challenging Research (Exploratory)

    Institution: Tohoku University

    2021/07/09 - 2023/03/31

  4. Study on neural mechanism of swallowing by imaging

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

    Category: Grant-in-Aid for Scientific Research (B)

    Institution: Tohoku University

    2020/04/01 - 2023/03/31

  5. Molecular physiological study of impairment in endosome system

    ANDO KEIKO

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    2017/04/01 - 2021/03/31

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    In this study, we focused on vps45 gene, which is one of the causative genes identified in severe congenital neutropenia (SCN). As an model animal, we used the nematode Caenorhabditis elegans (C. elegans) and conducted molecular genetic and molecular physiological studies of vps45. (1) To identify novel genes involved in vps45, we conducted genetic screenings for suppressor mutations of a vps45 mutant and obtained multiple suppressor mutant alleles. (2) We have developed a transgenic animal habouring human vps45 mutations in severe congenital neutropenia. (3) We developed a calcium imaging system to analyze calcium dynamics in apoptotic cells and neural activity in the SCN disease model.

  6. Development of Fluorescent Probes with Molecular Evolution Engineering

    NAKAI JUNICHI

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (S)

    Category: Grant-in-Aid for Scientific Research (S)

    2015/05/29 - 2020/03/31

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    Up until now, gene-encoded imaging probes were created using known protein fragments that bind to the molecule of interest to be detected. In this study, we applied molecular evolution engineering to develop a technology to create a new imaging probe using a peptide aptamer library or a small molecule antibody with a completely new sequence. In connection with this, we have developed technology for visualizing biological phenomena and evolutionary engineering technology such as immuno-PCR method. The developed technology is useful for elucidation of biological phenomena and medical treatment.

  7. Study of neuronal network mechanism for habit learning using highly sensitive calcium probe

    OHKURA Masamichi

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

    Category: Grant-in-Aid for Scientific Research (B)

    Institution: Saitama University

    2014/04/01 - 2018/03/31

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    To enable visualization and manipulation of neuronal network activities in zebrafish, we developed transgenic zebrafish expressing probes such as high-performance genetically-encoded fluorescent calcium indicators (improved G-CaMPs). We established an experimental system for quantitative calcium imaging of zebrafish brain region in response to visual stimuli, using transgenic fish expressing an improved green calcium probe G-CaMP and a red fluorescent protein.

  8. A study of neural circuit mechanism of voluntary behavior in C. elegans

    GENGYO-ANDO Keiko, NAKAI Junichi, OHKURA Masamichi, TAKAGI Shin

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research

    Category: Grant-in-Aid for Challenging Exploratory Research

    Institution: Saitama University

    2015/04/01 - 2017/03/31

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    Animals exhibit voluntary behaviors, but their neural mechanisms are not well understood. In this study, we developed a new imaging system, ICaST, which combines an automatic tracking system and a fast-scanning laser confocal microscope, to image neurons of interest in freely behaving C. elegans. Using ICaST in conjunction with an improved G-CaMP7, we conducted Ca2+ imaging of a freely moving animal at high magnification while automatically tracking the target in the microscope's field of view. We identified several neurons in the head ganglia that act before or during spontaneous backward locomotion. We also developed a system for optogenetic stimulation and simultaneous imaging by concurrent use of G-CaMP and ChR2. Our new approach will provide a powerful platform for studying the neural circuit mechanisms of C. elegans behaviors and has potential for use in other animals.

  9. Imaging analysis of neural circuit involved in voluntary behaviors in C. elegans

    GENGYO-ANDO Keiko, NAKAI Junichi, OHKURA Masamichi, HASHIMOTO Kouichi

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research

    Category: Grant-in-Aid for Challenging Exploratory Research

    Institution: Saitama University

    2013/04/01 - 2015/03/31

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    Most Animals can initiate and regulate voluntary behaviors in the absence of external stimuli, but the mechanism underlying decision-making is largely unknown. To elucidate the molecular and neural mechanism of these behaviors, we focused on C. elegans, which have a simple brain consisting of only 302 neurons and transparent body. Using our recently developed G-CaMP6-8, green genetically encoded calcium indicators (GECIs), we developed a system that allowed systematic imaging and analysis of the neural activity during spontaneous locomotion. We further designed R-CaMP2, a high-affinity, fast, red GECI, and successfully achieved dual-color imaging and optical stimulation in combination with green GECIs and channelrhodopshin 2 in freely moving C. elegans.

  10. Next generation photostimulation system using tunable laser

    NAKAI Junichi, ANDO Keiko

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research

    Category: Grant-in-Aid for Challenging Exploratory Research

    Institution: Saitama University

    2013/04/01 - 2014/03/31

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    In this study we developed a tunable wavelength photo-stimulation equipment. We could generate second harmonic waves ranging from ~400 nm to ~500 nm with a fun-out type periodically polarized crystal. So this equipment can photo-stimulate GFP, channelrhodopsin, and many other photosensitive molecules. In the system we also equipped a pair of potassium tantalate niobate (KTN) crystals as a tunable lens, an electro-optic device that changes its refractive index by voltage. By changing the voltage which applied to the tunable KTN lens, focus changed within ~20 microseconds. The speed of focus change was about 500~1000 times faster than that of the conventional piezo focuser. This technique can be applicable not only to scientific researches including brain science but also industrial field such as laser processing and laser measurement.

  11. 線虫の出力系回路における神経活動の可視化と解析

    安藤 恵子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 新学術領域研究(研究領域提案型)

    Category: 新学術領域研究(研究領域提案型)

    Institution: 埼玉大学

    2011/04/01 - 2013/03/31

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    ロコモーションは哺乳動物から無脊椎動物まで広く認められる周期的な運動であるが、神経回路がどのように運動パターンを生成し制御するのかについてはよくわかっていない。本研究は、我々の研究グループで新たに開発した改良型G-CaMPを線虫に応用し、運動中の個体における回路活動の定量的評価システムを確立するとともに、そのシステムを用いて出力系回路のイメージング解析を行い運動制御機構を明らかにすることを目的とした。 本年度の研究実施計画に基づいて実験を行い、以下の研究結果を得た。①我々が新たに開発した蛍光Ca2+センサーG-CaMP6およびG-CaMP7を線虫に応用し、細胞活動を高感度で再現性良く測定できる遺伝子改変動物を樹立した。G-CaMP6を線虫の後退運動で活性化するアセチルコリン作動性運動ニューロンに発現させたところ、従来のG-CaMPと比較して後退運動時に約2倍の蛍光強度変化を示し、in vivoで性能の向上が認められた②線虫の体の一部をパターン認識により自動追尾し、運動中の神経活動のリアルタイムレシオ蛍光画像と透過像を同時に撮像できるイメージングシステムを開発した(東北大・橋本浩一先生との共同研究)。③周期性運動におけるGABAの役割を明らかにするため、野生型およびGABA欠損変異体の前進運動および後退運動時の筋のCa2+動態を解析した。野生型では、前進・後退運動で筋細胞間を規則的に伝播するCa2+波が観察されたが、GABA欠損変異体では、後退時にCa2+波の伝播に異常が認められた。④運動ニューロンの発火パターンと筋細胞の出力パターンの機能的連関を明らかにするために、チャネルロドプシンを用いて運動ニューロンを光刺激した際の筋の応答をCa2+イメージングにより解析する系を確立した。

  12. Development of a next-generation photo-stimulation device

    NAKAI Junichi, ANDO Keiko, OHKURA Masamichi

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research

    Category: Grant-in-Aid for Challenging Exploratory Research

    Institution: Saitama University

    2012 - 2012

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    In this study we developed a microscope equipment with which photosensitive molecules can be stimulated. In the equipment a pair of potassium tantalate niobate (KTN) crystals were used as a tunable lens, an electro-optic device that changes its refractive index by voltage. By changing the voltage which applied to the tunable KTN lens focus changed within ~23 microseconds. The speed of focus change was about 500~1000 times faster than that of the conventional piezo focuser. This technique can be applicable not only to scientific researches including neuroscience but also industrial field such as laser processing.

  13. 線虫を用いた環境ホルモンの迅速な生体評価系の開発

    安藤 恵子

    System: 産学が連携した研究開発成果の展開 研究成果展開事業 研究成果最適展開支援プログラム(A-STEP) 探索タイプ

    Institution: 埼玉大学

    2011 - 2012

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    我々はライフサイクルが短く培養の容易な線虫を用いて環境ホルモンの簡便な生体評価系を開発している。本研究課題では、環境ホルモンの女性ホルモン様作用を生体外から生きたまま検出・評価するアッセイ系を構築するため、蛍光蛋白質遺伝子を導入した線虫の有用株を用いてin vivoでの光学的評価系の開発を行った。その結果、線虫を利用した光学的測定法が環境ホルモンの新たな生体評価系として有用である可能性が示された。この研究開発を基に非侵襲的な光学測定法が完成すれば、高速・低コストの生体評価系として水質、土壌などの環境調査や医薬、食品などの産業界に寄与できると期待される。

  14. STUDY OF SYNAPTIC MODULATORY MECHANISMS IN RESPONSE TO STRESS MEDIATED BY 5-HT2A RECEPTOR

    OHKURA Masamichi, NAKAI Junichi, ANDO Keiko

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Saitama University

    2010 - 2012

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    To enable detection of small calcium signals of neurons in response to single action potentials or synaptic inputs, we developed high-performance genetically-encoded fluorescent calcium indicators (improved G-CaMPs and R-CaMPs). We also established an experimental system for simultaneous photo-stimulation and fluorescence imaging of C. elegans expressing channelrhodopsin-2 in the HSN neuron and GFP-labeled 5-HT^<2A> or an improved G-CaMP in the vulval muscle.

  15. Functional study of Munc18 mutations associated with epilepsy

    ANDO Keiko, NAKAI Junichi, OHKURA Masamichi

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Saitama University

    2010 - 2012

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    To elucidate the molecular mechanism of intractable epilepsy, we developed C. elegans models having Munc18-1 mutations associated with Ohtahara syndrome (OS) known as early infantile epileptic encephalopathy (EIEE). We found that the Munc18-1 mutations resulted in behavioral defects such as paralysis and epileptic-like convulsions, and abnormalities in synaptic transmission. We also developed the optical measurement system of neural function using in vivo imaging and optogenetics. These disease models and optical technique can contribute to the understanding of the molecular pathogenesis and drug discovery for epilepsy.

  16. 線虫遺伝子破壊による低分子量G蛋白質RABファミリーのゲノム機能解析

    安藤 恵子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 特定領域研究

    Category: 特定領域研究

    2008 - 2009

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    低分子量G蛋白質Rabのアイソフォームはヒトでは60種類以上存在し、Rasスーパーファミリーの中で最大のサブファミリーを形成しているが、詳細な機能解析が進んでいる分子はごくわずかである。線虫Rab遺伝子は哺乳類Rabの約半数であり、相同遺伝子の重複が少なくシンプルな遺伝子構成をしているため解析が行ないやすいと考えられる。本研究課題ではRab分子の体系的な機能解明に向けて、TMP/UV法により線虫の全Rab遺伝子のノックアウト変異体株を樹立した。これらの変異体株について、個体の生存、稔性、発生、運動・行動、薬剤感受性などの表現型を観察し、Rab表現型のデータベース化を進めた。さらにトランスジェニックマーカーを用いて、各変異体バックグラウンドにおけるエンドサイトーシス経路、エキソサイトーシス経路、およびオルガネラの形態を解析した。これらの解析から各Rabメンバーについて普遍的な細胞機能と特殊化した細胞機能を担うタイプへの遺伝学的な分類が可能となった。また、エンドサイトーシス経路においてRabエフェクター分子であるRabenosyn-5を介したRab-5とSec1/Munc18分子との機能的連関を明らかにし、制御因子群を含めた解析に研究対象を発展させた。現在、カルシウムイメージングによって変異体の神経機能を解析・評価する生体アッセイ系の構築を進めている。

  17. Functional analysis of Rab proteins involved in endocytic transport in multicellular organism.

    ANDO Keiko

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Tokyo Women's Medical University

    2007 - 2009

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    A small G protein, Rab, is a major protein family which controls membrane traffic in eucaryotes. There are more than 60 members of Rab in the human genome, however, the biological functions of these proteins are not well understood. To clarify the physiological roles of Rab proteins in the endocytic transport, we isolated deletion mutants of genes encoding Rabs and their cooperating proteins in C.elegans. We systematically performed endocytosis assays using these mutations and identified proteins involved in endocytic transport in the multicellular organism.

  18. 線虫遺伝子破壊による低分子量G蛋白質RABファミリーのゲノム機能解析

    安藤 恵子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 特定領域研究

    Category: 特定領域研究

    Institution: 東京女子医科大学

    2006 - 2007

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    Rabは酵母からほ乳類まであらゆる真核細胞で保存されている低分子量G蛋白質でありさまざまな小胞輸送経路を制御することが知られている。しかしヒトやマウスでは60種以上もの異なるRab蛋白質が存在するためその生理機能は不明なものが多い。本研究課題では線虫Rabファミリーの体系的な逆遺伝学的解析により、Rab蛋白質の個体レベルでの生理機能を明らかにすることを目的としている。平成19年度は1.Rab遺伝子変異体の作成と株化、2.Rab遺伝子変異体の表現型解析、3.Rab遺伝子の発現解析を行った。線虫ゲノム上にはヒトRabの約半分に相当する29個のRab遺伝子が存在する。TMP/UV法で線虫ゲノム内にランダムに欠失変異を導入したmutant bankを各Rab遺伝子のプライマーでPCRスクリーニングし、欠失変異体を分離した。欠失部位のシークエンス解析を行い、エクソン配列を欠失していることを確認後、野生型線虫と数回戻し交配を行い、二次的な変異を取り除いた。当初計画通り、線虫全Rab遺伝子の欠失変異体を確立することができた。表現型解析の結果、酵母からヒトまで保存されているRab遺伝子変異体はほとんどが致死となり、ハウスキーピング遺伝子としての役割をもつと考えられた。一方、多細胞動物で獲得されたRab遺伝子の変異体はほとんどが生存可能であることがわかった。これらのRabは特定の組織や細胞における特殊な機能をもつ可能性や、サブファミリー間での機能相補の可能性が考えられる。また、GFP融合Rab遺伝子をもつトランスジェニック線虫を体系的に作製する方法を確立し、Rab遺伝子の発現解析を行った。Rab5やRab7などユビキタスな発現パターンを示すものや、Rab3やRab27など組織特異的な発現パターンを示すものがあり、現在各変異体表現型との対応付けを行っている。

  19. 線虫vps遺伝子群の網羅的遺伝子破壊によるリソソームの構築と輸送システムの解明

    安藤 恵子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 萌芽研究

    Category: 萌芽研究

    Institution: 東京女子医科大学

    2004 - 2005

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    酵母や培養細胞系などにより現在までに蓄積されているリソソーム/液胞系の知見を多細胞系で検証し、個体におけるリソソーム/液胞系のより高次な生理的意義を明らかにすることを目的として以下のような解析を行った。 (1)線虫vps遺伝子のノックアウト変異体の分離 液胞蛋白質輸送に関わる酵母変異体はvps遺伝子としてだけではなくさまざまな遺伝学的スクリーニングで同定されており、pep、vamなどについてもスクリーニングの対象にした。また、酵母では変異体として同定されていないが輸送系で重要な蛋白質ドメインをもつものに関してもスクリーニングの対象にした。変異体の分離は欠失変異をランダムに導入し目的とする欠失変異をPCRでスクリーニングするTMP/UV法を用いた(Gengyo-Ando & Mitani,2000)。分離した変異体は以下の通りである。(A)Sec1/Munc18;VPS33ホモログ2アリル,VPS45ホモログ1アリル(B)Syntaxin ; PEP12ホモログ3アリル,TLG2ホモログ1アリル,VAM3ホモログ1アリル(C)RabGTPase;RABホモログ15アリル(D)dynamin;VPS1ホモログ2アリル(E)VPS9ホモログ3アリル(F)PEP3/VPS18ホモログ1アリル(G)VPS39/VAM6/VPS3ホモログ1アリル(H)retromoer;VPS26ホモログ1アリル(I)VPS54ホモログ2アリル (2)変異部位の同定と変異体の維持 各変異体から欠失領域を含むPCRフラグメントを精製し、direct sequencing法で欠失領域を同定した。遺伝子のコード領域を数百〜2kb程度欠いた変異体が得られた。野生型株との戻し交配および致死変異体のバランサー導入を行った。 (3)変異体の表現型と機能解析 得られた変異体の半数以上がホモ接合体として維持不可能であり、vps遺伝子群の多くは動物個体の生存や発生に必須の遺伝子であると考えられた。さらに(A)および(B)の遺伝子変異体についてトフンスジェニックマーカーを用いた解析を行ったところ、ゴルジ体からリソソームへの輸送だけでは細胞膜からリソソームへのエンドサイトーシス経路にも輸送異常を示す変異体があることがわかった。 本研究課題を遂行することにより、さまざまなvps遺伝子群の遺伝的に安定した株が得られ、トランスジェニック解析を駆使した各々の蛋白質の機能解析を行なうための基盤作りができたと考えられる。

  20. Functional analysis of Sec1/Munc-18 family involved in membrane traffic

    ANDO Keiko

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Tokyo Women's Medical University School of Medicine

    2002 - 2003

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    The docking/fusion of transport vesicles mediated by the SNARE proteins is thought to be regulated by Sec1/Munc-18 (SM) proteins. The function of SM proteins is less well understood but their importance is emphasized by the blocks of general membrane trafficking and neurotransmitter release caused by mutations in SM proteins. There are 5 members of SM genes on the C.elegans genome, in addition to unc-18 regulating neurotransmitter release. To investigate systematically molecular structure and function of the Sec1/Munc-18 in multicellular organism, we isolated deletion mutations of all C.elegans SM proteins by TMP/UV method (K.Gengyo-Ando and S.Mitani, 2000). We are focusing on the C.elegans vps45 (Ce-vps45) whose orthologous protein in yeast plays an important role in membrane trafficking from the Golgi to vacuole. In this work, we reported that the putative null mutation of Ce-vps45, tm246, showed a maternal-effect as larval lethal phenotype, and this phenotype was rescued when Ce-vps45 cDNA was specifically expressed in the intestine. To visualize specific membrane trafficking pathway, we performed transgenic analyses using several fluorescent reporters in the mutant background. We found that tm246 mutation blocked the targeting of cathepsin D/EGFP fusion protein to gut granules. These results suggested that Ce-vps45 gene products may function in membrane trafficking from the Golgi to lysosome in mainly intestinal cells where lysosome is highly developed. Ce-vps45 may also be required for endocytic pathway because tm246 mutant showed a coelomocyte uptake defective (Cup) phenotype (H.Fares and I.Greenwald, 2001) in restrictive temperature. Our data demonstrate that Ce-vps45 regulating two different membrane trafficking events in C.elegans.

  21. 逆遺伝学的アプローチによる線虫UNC-18ファミリーの系統的機能解析

    安藤 恵子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 奨励研究(A)

    Category: 奨励研究(A)

    Institution: 東京女子医科大学

    2001 - 2002

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    Secl/Munc-18ファミリーは酵母から哺乳類神経系に至るまで進化的に保存された小胞輸送機能分子である。線虫ゲノム上には6つのSecl/Munc-18蛋白質が見い出されている。申請者は逆遺伝学的解析が適用できる線虫をモデル動物として用いることによりSecl/Munc-18蛋白質の系統的な機能解析を行い、多細胞系の膜輸送におけるSecl/Munc-18ファミリーの生理的役割について明らかにしていくことを計画した。過去2年間で申請者はゴルジ体から液胞/リソソームへの膜輸送に関与すると考えられるvps45ホモログ(Ce-vps45)について当初研究計画に基づいて実験を行い、以下のような結果を得た。Ce-vps45::EGFP融合遺伝子をレポーターに用いたトランスジェニック解析によりほぼすべての発生ステージにわたり神経、筋肉、表皮、腸管等多くの組織で発現が認められた。Ce-vps45のこのようなubiquitousな発現パターンはvps45がリソソームへの膜輸送に関与するという知見と矛盾しないように思われる。Ce-vps45の機能を明らかにするためTMP/UV法を用いてコード領域に約1.2kbの欠失を持つ変異体tm246を分離した。欠失は開始コドンを含んでいるため、おそらくnull型変異であると推測された。遺伝学的解析からtm246は母性効果のある温度感受性劣性幼虫致死変異であることを見い出した。tm246ホモ接合体は低温生育下では生存可能であるが、高温生育下ではほぼL1期に発生停止となった。この時期は自家蛍光物質の蓄積などで推測されるリソソームが発達する時期に一致している。また、制限温度で生育した変異体の腸管細胞内ではリソソームマーカーである線虫カテプシンD/EGFP融合蛋白質の異常なaggregatesが認められ、リソソーム経路の機能障害が示唆された。

  22. 神経伝達物質放出に関与する線虫UNC-18ファミリーの機能解析

    安藤 恵子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 奨励研究(A)

    Category: 奨励研究(A)

    Institution: 東京女子医科大学

    1998 - 1999

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    線虫ゲノム上に存在するunc-18類似遺伝子の構造と機能を明らかにする目的で本年度の研究実施計画に基づき(1)ゲノム上に同定された4つのアイソフォームのうちの1つのB0303.9についてcDNA塩基配列決定およびレポーターアッセイによる発現解析、(2)unc-18ファミリーの系統的逆遺伝学的解析のための高効率遺伝子破壊法の開発とミュータントバンクの作成を行った。 (1)B0303.9全長cDNAクローンを得、塩基配列を決定した。B0303.9は603アミノ酸をコードすることが予測され、他生物種unc-18ファミリーと20%程度の相同性(同一アミノ酸)を示した。またB0303.9は腸管細胞、excretory canal細胞、CAN神経細胞等で発現が認められ、これらの分泌組織で働いていると考えられた。 (2)線虫の逆遺伝学的解析法として化学変異原でゲノムに欠失変異を導入し、PCRで目的とする欠失変異体を選別する方法が適用されているが変異体分離の頻度が低いのが難点であった。そこでさまざまな条件検討を行い、従来法よりも高効率な方法を開発した(論文印刷中)。線虫凍結ミュータントバンクを作成し、パイロットスクリーニングを行ったところ、1つのアイソフォームC44C1.4の欠失変異体が得られた。さらにバンクサイズを大きくし、すべてのアイソフォームの欠失変異体を分離する予定である。

  23. 神経伝達物質遊離に関与するunc-18マウス相同遺伝子の構造と機能

    安藤 恵子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 奨励研究(A)

    Category: 奨励研究(A)

    Institution: 理化学研究所

    1994 - 1994

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    本研究実施計画に基づきマウスunc-18相同遺伝子の同定を試み、マウス脳cDNAライブラリーからunc-18相同蛋白質をコードする2種類のcDNAクローン(unc-18α,unc-18β)を単離することに成功した。unc-18αはアミノ酸配列全長にわたり64.7%,unc-18αは44.9%の相同性をもち、推定分子量、アミノ酸組成共、線虫UNC-18蛋白質と似通っていることが明らかになった。データベース検索を行った結果、unc-18α蛋白質は神経前終末膜に局在するsyntaxinの特異的結合蛋白質として同定されたラットMunc-18と同一の蛋白質であり、unc-18β蛋白質は末だ報告されていない新しいタイプのUNC-18アイソフォームであることが判明した。そこで我々は、これらの相同遺伝子をsynap(syntaxin associated protein)1,synap2と命名した。ノーザンブロット解析では、synap1は脳特異的に、synap2は脳、肝臓、腎臓、心臓、脾臓、筋肉、精巣など各組織で発現しており、組織発現特異性が異なることがわかった。マイクロインジェクションによる線虫unc-18突然特異体機能相補実験を行ったところ、synap1トランスジェニック線虫では表現型回復が認められたのに対し、synap2トランスジェニック線虫では回復は認められなかった。マウス相同遺伝子の発現特異性と機能回復実験からsynap1はunc-18に対する機能的相同遺伝子であり、synap2は機能的特性の異なる相同遺伝子であると考えられる。 最近の世界的な研究報告からsyntaxinは膜融合のターゲット膜蛋白質と考えられており、synap蛋白質同様、発現特異性の異なる複数のアイソフォームの存在が知られている。したがってsynap蛋白質ファミリーは特異的膜融合に関わる新しい細胞質性因子であると考えられる。

  24. 線虫アセチルコリン異常蓄積変異遺伝子unc-18の構造と機能

    安藤 恵子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 奨励研究(A)

    Category: 奨励研究(A)

    Institution: 理化学研究所

    1993 - 1993

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    本研究はシナプスにおける情報伝達機構解明を目的とする。線虫C.elegansのunc-18遺伝子は68Kの親水性蛋白質をコードし、unc-18遺伝子変異により、行動異常、アセチルコリンエステラーゼ抵抗性、アセチルコリン異常蓄積等の表現型がみられる。また、酵母の細胞内小胞輸送に関与するSecl/Slyl/Slplとの類似性から、UNC-18蛋白質は神経伝達物質放出に関わる新しい因子であると推論された。特に変異によりsecretory vesicleの蓄積を起こすseclと似ていることから、神経細胞においてsynaptic vesicleの神経終末への輸送やexocytosisに関与している可能性が考えられた。unc-18の発現パターンを抗UNC-18抗体による免疫染色で調べたところ、腹部神経索を構成する運動神経細胞の細胞体と軸索が強く染色され、頭部ガングリオンの一部のん神経細胞でも特異的に発現が認められた。unc-18遺伝子変異はアセチルコリン異常蓄積を引き起こすが、コリン作働性神経細胞だけではなく、セロトニン作働性、GABA 作働性神経細胞でも発現していることから、一般的な神経伝達物質放出に関与することが示唆される。 また、本年度の研究実施計画に基づき、UNC-18蛋白質の機能ドメインを同定するため線虫C.elegansの近縁種C.briggsaeのゲノムライブラリーを作製し、unc-18相同遺伝子をクローニングした。DNA塩基配列から予測されるアミノ酸配列は高度に保存されており(97.5%同一)、C.elegansUNC-18蛋白質に対する抗血清と交叉反応を示した。線虫のシナプス機能に関与する遺伝子には哺乳動物遺伝子と相同性を示すものがあることから、マウスunc-18相同遺伝子のクローニングを行った。弱い条件下でのサザン、ノーザンハイブリダイゼーションによりシグナルが検出されなかったため、Secl/Slyl/Slplとの相同領域をプライマーとして脳PolyA+RNAのRT-PCRを行った。unc-18とアミノ酸レベルで70%程度相同な2つの分子種が得られた。これら2つのマウス相同遺伝子と2つの線虫遺伝子のコードするアミノ酸配列を比較することにより、高度に保存された配列が決定された。また、マウス相同遺伝子のノーザンブロット解析から、一方は脳特異的な4.0kbの転写産物がみられ、他方は各組織に2.8kbの転写産物が検出された。この結果はunc-18相同遺伝子がシナプスにおけるregulated secretionだけでなく真核細胞共通に起こるconstitutive secretionにも関与することを示唆する。現在、これらの相同遺伝子が線虫unc-18突然変異を機能相補し得るかどうか検討中である。

  25. 線虫Caenorhabditis elegansの太い線維形成機構

    安藤 恵子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 奨励研究(特別研究員)

    Category: 奨励研究(特別研究員)

    Institution: 岡山大学

    1990 - 1990

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