The chimeric gene atp6c confers cytoplasmic male sterility in maize by impairing the assembly of mitochondrial ATP synthase complex

第一作者：Huili Yang

第一单位：河南农业大学

通讯作者：Jihua Tang

 Abstarct 

背景回顾：Cytoplasmic male sterility (CMS) is a powerful tool for the exploitation of hybrid heterosis and the study of signaling and interactions between the nucleus and the cytoplasm. 

细胞质雄性不育（CMS）是利用杂种优势和研究核质信号与互作的有力工具。

提出问题：C-type CMS (CMS-C) in maize has long been used in hybrid seed production, but the underlying sterility factor and its mechanism of action remain unclear. 

玉米中的C型CMS长期以来被用于杂交种子的生产，但是潜在的育性因子及其作用机制仍不清楚。

主要研究：In this study, we demonstrate that the mitochondrial gene atp6c confers male sterility in CMS-C maize. 

本文中，作者发现线粒体基因atp6c赋予了C型CMS玉米的雄性不育。

结果1-ATP6C功能：The ATP6C protein showed stronger interactions with ATP8 and ATP9 than ATP6 in the assembly of F1Fo-ATP synthase (F-type ATP synthase, ATPase), thereby reducing the quantity and activity of assembled F1Fo-ATP synthase. By contrast, the quantity and activity of the F1' component were increased in CMS-C lines. 

相比于F型ATP酶F1Fo-ATPase组装体中的ATP6蛋白，ATP6C蛋白和ATP8/9的互作更强，因此降低了F1Fo-ATPase组装体的质量与活性。相反，在CMS-C株系中F1’组分的质量和活性有所增加。

结果2-atp6c介导CMS-C的机制：Reduced F1Fo-ATP synthase activity caused accumulation of excess protons in the inner membrane space of the mitochondria, triggering a burst of reactive oxygen species (ROS), premature programmed cell death of the tapetal cells, and pollen abortion. 

F1Fo-ATPase活性的降低会导致线粒体内膜积累过量的质子，从而诱发活性氧物质（ROS）的爆发，最终导致绒毡层细胞的提前细胞程序性死亡、花粉败育。

结论：These findings locate the sterility gene, document the contribution of ATP6C to F1Fo-ATP synthase assembly, and provide novel insights into the molecular mechanisms of male sterility in CMS-C maize.

本文的研究结果定位到了玉米C型CMS的关键基因，揭示了其作用于F1Fo-ATPase组装的功能，为玉米C型CMS的雄性不育分子机制提供了新的视野。

** 汤继华 **

doi: https://doi.org/10.1016/j.molp.2022.03.002

Journal: Molecular Plants

Published date: March 08, 2022