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

研究成果: Contribution to journalArticle査読

13 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)374-387
ページ数14
ジャーナルDevelopmental Cell
25
4
DOI
出版ステータス出版済み - 5 28 2013
外部発表はい

All Science Journal Classification (ASJC) codes

  • 分子生物学
  • 生化学、遺伝学、分子生物学(全般)
  • 発生生物学
  • 細胞生物学

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