| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| 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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