Role of vacuolar-type proton pump in compensated cell enlargement
| Project/Area Number |
21770036
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Plant molecular biology/Plant physiology
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| Research Institution | Tokyo Gakugei University |
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Principal Investigator |
FERJANI Ali Tokyo Gakugei University, 教育学部, 助教 (20530380)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2009: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 葉器官サイズ制御 / 細胞増殖 / 細胞伸長 / fugu5変異体 / 補償作用 |
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| Research Abstract |
A longstanding question in biology is how organ size is predetermined. Compensation is a key, yet unsolved phenomenon, whereby decreased cell number below some threshold triggers enhanced post-mitotic cell expansion in leaf primordia. Thus providing a model case to investigate leaf-size control. Among the Arabidopsis mutants that exhibit compensation, here I focused on fugu5 mutant that is defective in vacuolar-type H^+-pyrophosphatase (H^+-PPase). I clearly demonstrated that high accumulation of PPi in the cytosol mediates gluconeogenesis compromise in fugu5, providing evidence that PPi hydrolysis is the major role of FUGU5 in vivo. Also, I conducted a large-scale screening of enhancers, repressors and suppressors of fugu5 mutant and identified three mutant lines that affect cell expansion in fugu5 in different manners. Finally, I found that V-ATPase is implicated in excessive cell enlargement observed in fugu2-1 and KRP2 o/e.
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Report
(3 results)
Research Products
(30 results)
