摘要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.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.In this study,we demonstrate that the mitochondrial gene atp6c confers male sterility in CMS-C maize.The ATP6C protein shows stronger interactions with ATP8 and ATP9 than ATP6 during the assembly of F1F0-ATP synthase(F-type ATP synthase,ATPase),thereby reducing the quantity and activity of assem-bled F1Fo-ATP synthase.By contrast,the quantity and activity of the F1'component are increased in CMS-C lines.Reduced F1F0-ATP synthase activity causes 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 tapetai cells,and pollen abortion.Collectively,our study identifies a chimeric mitochondrial gene(ATP6C)that causes CMS in maize and documents the contribution of ATP6C to F1F0-ATP synthase assembly,thereby providing novel insights into the molecular mechanisms of male sterility in plants.