Cytoplasmic male sterility of rice with boro II cytoplasm is caused by a cytotoxic peptide and is restored by two related PPR motif genes via distinct modes of mRNA silencing
Cytoplasmic male sterility of rice with boro II cytoplasm is caused by a cytotoxic peptide and is restored by two related PPR motif genes via distinct modes of mRNA silencing
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DOI：
10.1105/tpc.105.038240
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发表时间：
2006-03-01
期刊：
影响因子：
11.6
通讯作者：
Liu, YG
中科院分区：
文献类型：
--
作者：
Wang, ZH;Zou, YJ;Liu, YG
细胞质雄性不育（CMS）和核控育性恢复是植物广泛存在的生殖特征，为利用作物杂种优势提供了有用的工具。然而，这种细胞质核相互作用的分子机制仍不清楚。在这里，我们表明，在水稻（水稻）与Boro II细胞质的异常线粒体开放阅读框，orf 79，与一个重复的atp 6（B-atp 6）基因共转录，并编码一个细胞毒性肽。orf 79在不育系和转基因水稻植株中的表达导致配子体雄性不育。免疫印迹分析表明ORF 79蛋白在小孢子中特异性积累。两个育性恢复基因，Rf 1a和Rf 1b，被确定为一个多基因簇的成员，编码pentatricopeptide重复蛋白的经典位点Rf-1。RF 1A和RF 1B都靶向线粒体，并且可以通过双顺反子B-atp 6/orf 79 mRNA的内切核酸裂解（RF 1A）或降解（RF 1B）阻断ORF 79的产生来恢复雄性生育力。在两个恢复子的存在下，RF 1A在mRNA加工中上位于RF 1B。我们还表明，RF 1A在促进atp 6 mRNA的编辑中起着额外的作用，独立于其切割功能。
Cytoplasmic male sterility (CMS) and nucleus-controlled fertility restoration are widespread plant reproductive features that provide useful tools to exploit heterosis in crops. However, the molecular mechanism underlying this kind of cytoplasmic nuclear interaction remains unclear. Here, we show in rice (Oryza sativa) with Boro II cytoplasm that an abnormal mitochondrial open reading frame, orf79, is cotranscribed with a duplicated atp6 (B-atp6) gene and encodes a cytotoxic peptide. Expression of orf79 in CMS lines and transgenic rice plants caused gametophytic male sterility. Immunoblot analysis showed that the ORF79 protein accumulates specifically in microspores. Two fertility restorer genes, Rf1a and Rf1b, were identified at the classical locus Rf-1 as members of a multigene cluster that encode pentatricopeptide repeat proteins. RF1A and RF1B are both targeted to mitochondria and can restore male fertility by blocking ORF79 production via endonucleolytic cleavage (RF1A) or degradation (RF1B) of dicistronic B-atp6/orf79 mRNA. In the presence of both restorers, RF1A was epistatic over RF1B in the mRNA processing. We have also shown that RF1A plays an additional role in promoting the editing of atp6 mRNAs, independent of its cleavage function.