2016 Fiscal Year Final Research Report
ER-resident BH3-only protein, BNip1, induces apoptosis in response to excessive activation of vesicular transport in zebrafish photoreceptors
Project/Area Number |
26440128
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Developmental biology
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Research Institution | Okinawa Institute of Science and Technology Graduate University |
Principal Investigator |
Nishiwaki Yuko 沖縄科学技術大学院大学, 神経発生ユニット, 研究員 (20360620)
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Co-Investigator(Renkei-kenkyūsha) |
MASAI Ichiro 沖縄科学技術大学院大学, 神経発生ユニット, 准教授 (50242087)
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Keywords | BNip1 / 細胞死誘導 / 小胞輸送 |
Outline of Final Research Achievements |
Zebrafish beta-SNAP mutants show photoreceptor apoptosis through the activation of a BH3-domain containing SNARE protein, BNip1. BNip1 is a target-SNARE component of syntaxin18 SNARE complex, which normally regulates retrograde transport from Golgi to endoplasmic reticulum(ER). In this study, I found that the depletion of beta-SNAP activates BNip1-dependent apoptosis in zebrafish photoreceptors only in the early developmental stage when intracellular protein transport to the outer segment is active. Furthermore, our data indicate that the inhibition of protein transport to the outer segment rescues photoreceptor apoptosis in the beta-SNAP mutant. From these data, we propose that BNip1 functions as a safe guard mechanism that inhibits excessive activation of vesicular transport during photoreceptor differentiation.
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Free Research Field |
発生生物学
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