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A detrimental mitochondrial-nuclear interaction causes cytoplasmic male sterility in rice
A detrimental mitochondrial-nuclear interaction causes cytoplasmic male sterility in rice
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A detrimental mitochondrial-nuclear interaction causes cytoplasmic male sterility in rice
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A detrimental mitochondrial-nuclear interaction causes cytoplasmic male sterility in rice
A detrimental mitochondrial-nuclear interaction causes cytoplasmic male sterility in rice

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A detrimental mitochondrial-nuclear interaction causes cytoplasmic male sterility in rice
A detrimental mitochondrial-nuclear interaction causes cytoplasmic male sterility in rice
Journal Article

A detrimental mitochondrial-nuclear interaction causes cytoplasmic male sterility in rice

2013
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Overview
Yao-Guang Liu and colleagues identify the molecular basis of male sterility in the Wild Abortive CMS (CMS-WA) system that has been widely used for hybrid rice breeding. They report that a new mitochondrial gene, WA532 , confers male sterility because its protein product interacts with the mitochondrial protein COX11 and leads to cytoplasmic-nuclear incompatibility. Plant cytoplasmic male sterility (CMS) results from incompatibilities between the organellar and nuclear genomes and prevents self pollination, enabling hybrid crop breeding to increase yields 1 , 2 , 3 , 4 , 5 , 6 . The Wild Abortive CMS (CMS-WA) has been exploited in the majority of 'three-line' hybrid rice production since the 1970s, but the molecular basis of this trait remains unknown. Here we report that a new mitochondrial gene, WA352 , which originated recently in wild rice, confers CMS-WA because the protein it encodes interacts with the nuclear-encoded mitochondrial protein COX11. In CMS-WA lines, WA352 accumulates preferentially in the anther tapetum, thereby inhibiting COX11 function in peroxide metabolism and triggering premature tapetal programmed cell death and consequent pollen abortion. WA352-induced sterility can be suppressed by two restorer-of-fertility ( Rf ) genes, suggesting the existence of different mechanisms to counteract deleterious cytoplasmic factors. Thus, CMS-related cytoplasmic-nuclear incompatibility is driven by a detrimental interaction between a newly evolved mitochondrial gene and a conserved, essential nuclear gene.