| Project/Area Number |
16K07392
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Plant molecular biology/Plant physiology
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| Research Institution | Saitama University |
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Principal Investigator |
NISHIDA IKUO 埼玉大学, 理工学研究科, 教授 (40189288)
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 呼吸活性 / 低温成長 / リン脂質生合成の意義 / 呼吸 / COP活性 / AOP活性 / 外向きNAD(P)HデヒドロゲナーゼNDB2 / 低温生育改善 / 恒常的活性型AOX1a* / 光呼吸 / 早期花成 / COP経路 / AOP経路 / COX活性 / 低温生育阻害 / ホスファチジルエタノールアミン / pect1-4 / aox1a / 脂質 / 植物 / 生理学 |
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| Outline of Final Research Achievements |
The pect1-4 mutant that exhibits a 26% residual activity of CDP-ethanolamine biosynthesis shows pleiotropic mutant phenotypes, such as growth retardation at low temperature or short-day conditions and early flowering. In this study, we demonstrated that pect1-4 mutation causes downregulation of COP respiratory capacity, which in turn causes the growth retardation at low temperature or short-day conditions. Overexpression of constitutively active AOX1a* in pect1-4 mutants fully resumed the COP respiratory capacity and recovered from the growth retardation. On the other hand, pect1-4 AOX1a* plants partially recovered from the early flowering phenotype. Taken together, our results suggested that the pect1-4 mutant exhibits the pleiotropic mutant phenotypes via a respiratory capacity-dependent stress pathway and a non-stress pathway.
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| Academic Significance and Societal Importance of the Research Achievements |
ホスファチジルエタノールアミン（PE)はミトコンドリアなどの細胞内小器官の膜を構成するリン脂質であるが、その生合成を完全に阻害すると、細胞が生存できず、さらなる研究を阻んでいた。われわれは、PE生合成活性が野生型の1/4まで低下したpect1-4変異株を用いることにより、ミトコンドリアの機能低下によってもたらされる変異は、呼吸に依存したストレス経路と、呼吸に依存しない非ストレス経路によって引き起こされることをあきらかにした。
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