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Open syntaxin overcomes exocytosis defects of diverse mutants in C. elegans

Author

Listed:
  • Chi-Wei Tien

    (University Health Network
    University of Toronto)

  • Bin Yu

    (Huazhong University of Science and Technology)

  • Mengjia Huang

    (University Health Network
    University of Toronto)

  • Karolina P. Stepien

    (University of Texas Southwestern Medical Center
    University of Texas Southwestern Medical Center
    University of Texas Southwestern Medical Center)

  • Kyoko Sugita

    (University Health Network)

  • Xiaoyu Xie

    (University Health Network
    Dalian Medical University)

  • Liping Han

    (Dalian Medical University
    Dalian Medical University)

  • Philippe P. Monnier

    (University of Toronto
    University Health Network
    University of Toronto)

  • Mei Zhen

    (University of Toronto
    Mount Sinai Hospital
    University of Toronto)

  • Josep Rizo

    (University of Texas Southwestern Medical Center
    University of Texas Southwestern Medical Center
    University of Texas Southwestern Medical Center)

  • Shangbang Gao

    (Huazhong University of Science and Technology)

  • Shuzo Sugita

    (University Health Network
    University of Toronto)

Abstract

Assembly of SNARE complexes that mediate neurotransmitter release requires opening of a ‘closed’ conformation of UNC-64/syntaxin. Rescue of unc-13/Munc13 mutant phenotypes by overexpressed open UNC-64/syntaxin suggested a specific function of UNC-13/Munc13 in opening UNC-64/ syntaxin. Here, we revisit the effects of open unc-64/syntaxin by generating knockin (KI) worms. The KI animals exhibit enhanced spontaneous and evoked exocytosis compared to WT animals. Unexpectedly, the open syntaxin KI partially suppresses exocytosis defects of various mutants, including snt-1/synaptotagmin, unc-2/P/Q/N-type Ca2+ channel alpha-subunit and unc-31/CAPS, in addition to unc-13/Munc13 and unc-10/RIM, and enhanced exocytosis in tom-1/Tomosyn mutants. However, open syntaxin aggravates the defects of unc-18/Munc18 mutants. Correspondingly, open syntaxin partially bypasses the requirement of Munc13 but not Munc18 for liposome fusion. Our results show that facilitating opening of syntaxin enhances exocytosis in a wide range of genetic backgrounds, and may provide a general means to enhance synaptic transmission in normal and disease states.

Suggested Citation

  • Chi-Wei Tien & Bin Yu & Mengjia Huang & Karolina P. Stepien & Kyoko Sugita & Xiaoyu Xie & Liping Han & Philippe P. Monnier & Mei Zhen & Josep Rizo & Shangbang Gao & Shuzo Sugita, 2020. "Open syntaxin overcomes exocytosis defects of diverse mutants in C. elegans," Nature Communications, Nature, vol. 11(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-19178-x
    DOI: 10.1038/s41467-020-19178-x
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    Cited by:

    1. Shingo Hiroki & Hikari Yoshitane & Hinako Mitsui & Hirofumi Sato & Chie Umatani & Shinji Kanda & Yoshitaka Fukada & Yuichi Iino, 2022. "Molecular encoding and synaptic decoding of context during salt chemotaxis in C. elegans," Nature Communications, Nature, vol. 13(1), pages 1-15, December.

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