The BH3-Only SNARE BNip1 Mediates Photoreceptor Apoptosis in Response to Vesicular Fusion Defects

Yuko Nishiwaki, Asuka Yoshizawa, Yutaka Kojima, Eri Oguri, Shohei Nakamura, Shohei Suzuki, Junichi Yuasa-Kawada, Mariko Kinoshita-Kawada, Toshiaki Mochizuki, Ichiro Masai

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    9 Citations (Scopus)


    Intracellular vesicular transport is important for photoreceptor function and maintenance. However, the mechanism underlying photoreceptor degeneration in response to vesicular transport defects is unknown. Here, we report that photoreceptors undergo apoptosis in a zebrafish β-soluble N-ethylmaleimide-sensitive factor attachment protein (β-SNAP) mutant. β-SNAP cooperates with N-ethylmaleimide-sensitive factor to recycle the SNAP receptor (SNARE), a key component of the membrane fusion machinery, by disassembling the cis-SNARE complex generated in the vesicular fusion process. We found that photoreceptor apoptosis in the β-SNAP mutant was dependent on the BH3-only protein BNip1. BNip1 functions as a component of the syntaxin-18 SNARE complex and regulates retrograde transport from the Golgi to the endoplasmic reticulum. Failure to disassemble the syntaxin-18 cis-SNARE complex caused BNip1-dependent apoptosis. These data suggest that the syntaxin-18 cis-SNARE complex functions as an alarm factor that monitors vesicular fusion competence and that BNip1 transforms vesicular fusion defects into photoreceptor apoptosis.

    Original languageEnglish
    Pages (from-to)374-387
    Number of pages14
    JournalDevelopmental Cell
    Issue number4
    Publication statusPublished - May 28 2013

    All Science Journal Classification (ASJC) codes

    • Molecular Biology
    • Biochemistry, Genetics and Molecular Biology(all)
    • Developmental Biology
    • Cell Biology

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