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在拟南芥中,MORF9依赖性的特定质体RNA编辑在糖饥饿条件下抑制根的生长。

MORF9-dependent specific plastid RNA editing inhibits root growth under sugar starvation in Arabidopsis.

作者信息

Xie Yakun, Yu Jinfa, Tian Faan, Li Xue, Chen Xinyan, Li Yanyun, Wu Binghua, Miao Ying

机构信息

Fujian Provincial Key Laboratory of Plant Functional Biology, College of Life Sciences, Fujian Agriculture and Forestry University, Fuzhou, China.

出版信息

Plant Cell Environ. 2024 Jun;47(6):1921-1940. doi: 10.1111/pce.14856. Epub 2024 Feb 15.

Abstract

Multiple organellar RNA editing factor (MORF) complex was shown to be highly associated with C-to-U RNA editing of vascular plant editosome. However, mechanisms by which MORF9-dependent plastid RNA editing controls plant development and responses to environmental alteration remain obscure. In this study, we found that loss of MORF9 function impaired PSII efficiency, NDH activity, and carbohydrate production, rapidly promoted nuclear gene expression including sucrose transporter and sugar/energy responsive genes, and attenuated root growth under sugar starvation conditions. Sugar repletion increased MORF9 and MORF2 expression in wild-type seedlings and reduced RNA editing of matK-706, accD-794, ndhD-383 and ndhF-290 in the morf9 mutant. RNA editing efficiency of ndhD-383 and ndhF-290 sites was diminished in the gin2/morf9 double mutants, and that of matK-706, accD-794, ndhD-383 and ndhF-290 sites were significantly diminished in the snrk1/morf9 double mutants. In contrast, overexpressing HXK1 or SnRK1 promoted RNA editing rate of matK-706, accD-794, ndhD-383 and ndhF-290 in leaves of morf9 mutants, suggesting that HXK1 partially impacts MORF9 mediated ndhD-383 and ndhF-290 editing, while SnRK1 may only affect MORF9-mediated ndhF-290 site editing. Collectively, these findings suggest that sugar and/or its intermediary metabolites impair MORF9-dependent plastid RNA editing resulting in derangements of plant root development.

摘要

多细胞器RNA编辑因子(MORF)复合体被证明与维管植物编辑体的C到U RNA编辑高度相关。然而,MORF9依赖的质体RNA编辑控制植物发育和对环境变化响应的机制仍不清楚。在本研究中,我们发现MORF9功能丧失会损害PSII效率、NDH活性和碳水化合物生成,迅速促进包括蔗糖转运蛋白和糖/能量响应基因在内的核基因表达,并在糖饥饿条件下减弱根的生长。在野生型幼苗中,糖分充足会增加MORF9和MORF2的表达,并减少morf9突变体中matK - 706、accD - 794、ndhD - 383和ndhF - 290的RNA编辑。在gin2/morf9双突变体中,ndhD - 383和ndhF - 290位点的RNA编辑效率降低,而在snrk1/morf9双突变体中,matK - 706、accD - 794、ndhD - 383和ndhF - 290位点的RNA编辑效率显著降低。相反,过表达HXK1或SnRK1可促进morf9突变体叶片中matK - 706、accD - 794、ndhD - 383和ndhF - 290的RNA编辑率,这表明HXK1部分影响MORF9介导的ndhD - 383和ndhF - 290编辑,而SnRK1可能仅影响MORF9介导的ndhF - 290位点编辑。总的来说,这些发现表明糖和/或其中间代谢产物损害了MORF9依赖的质体RNA编辑,导致植物根系发育紊乱。

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