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Plant Cell Advance Online Publication
Published on February 17, 2006; 10.1105/tpc.105.038240

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Received September 28, 2005
Returned for revision December 14, 2005
Accepted January 12, 2006

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

Zhonghua Wang 1, Yanjiao Zou 1, Xiaoyu Li 1, Qunyu Zhang 1, Letian Chen 1, Hao Wu 1, Dihua Su 1, Yuanling Chen 1, Jingxin Guo 1, Da Luo 2, Yunming Long 1, Yang Zhong 3, and Yao-Guang Liu 1*

1 Key Laboratory of Plant Functional Genomics and Biotechnology of Guangdong Province, College of Life Sciences, South China Agricultural University, Guangzhou 510642, China
2 Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, Shanghai 200032, China; School of Life Science and Biotechnology, Shanghai Jiao Tong University, Shanghai 200030, China
3 School of Life Sciences, Fudan University, Shanghai 200433, China

* To whom correspondence should be addressed. E-mail: ygliu{at}scau.edu.cn.

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.






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