Plant Physiol.
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First published online May 27, 2005; 10.1104/pp.104.058347

Plant Physiology 138:965-976 (2005)
© 2005 American Society of Plant Biologists

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GENETICS, GENOMICS, AND MOLECULAR EVOLUTION

The AtRAD51C Gene Is Required for Normal Meiotic Chromosome Synapsis and Double-Stranded Break Repair in Arabidopsis1

Wuxing Li, Xiaohui Yang, Zhenguo Lin, Ljudmilla Timofejeva, Rong Xiao, Christopher A. Makaroff and Hong Ma*

Department of Biology and the Huck Institutes of the Life Sciences (W.L., Z.L., L.T., R.X., H.M.) and Intercollege Graduate Program in Plant Physiology (W.L., R.X., H.M.), the Pennsylvania State University, University Park, Pennsylvania 16802; Department of Chemistry and Biochemistry, Miami University, Oxford, Ohio 45056 (X.Y., C.A.M.); and Department of Gene Technology, Tallinn University of Technology, Tallinn 12618, Estonia (L.T.)

Meiotic prophase I is a complex process involving homologous chromosome (homolog) pairing, synapsis, and recombination. The budding yeast (Saccharomyces cerevisiae) RAD51 gene is known to be important for recombination and DNA repair in the mitotic cell cycle. In addition, RAD51 is required for meiosis and its Arabidopsis (Arabidopsis thaliana) ortholog is important for normal meiotic homolog pairing, synapsis, and repair of double-stranded breaks. In vertebrate cell cultures, the RAD51 paralog RAD51C is also important for mitotic homologous recombination and maintenance of genome integrity. However, the function of RAD51C in meiosis is not well understood. Here we describe the identification and analysis of a mutation in the Arabidopsis RAD51C ortholog, AtRAD51C. Although the atrad51c-1 mutant has normal vegetative and flower development and has no detectable abnormality in mitosis, it is completely male and female sterile. During early meiosis, homologous chromosomes in atrad51c-1 fail to undergo synapsis and become severely fragmented. In addition, analysis of the atrad51c-1 atspo11-1 double mutant showed that fragmentation was nearly completely suppressed by the atspo11-1 mutation, indicating that the fragmentation largely represents a defect in processing double-stranded breaks generated by AtSPO11-1. Fluorescence in situ hybridization experiments suggest that homolog juxtaposition might also be abnormal in atrad51c-1 meiocytes. These results demonstrate that AtRAD51C is essential for normal meiosis and is probably required for homologous synapsis.


1 This work was supported by the National Institutes of Health (grant no. R01 GM63871–01 to H.M.) and the National Science Foundation (grant nos. MCB–0092075 to H.M. and MCB–0322171 to C.A.M.). W.L. was partially supported by the Intercollege Graduate Program in Plant Physiology at the Pennsylvania State University. R.X. is supported by a University Graduate Fellowship from the Pennsylvania State University. H.M. gratefully acknowledges the support of the John Simon Guggenheim Memorial Foundation, the K.C. Wong Educational Foundation, and the Foreign Distinguished Young Scholar Award from the Chinese National Science Foundation.

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.104.058347.

* Corresponding author; e-mail hxm16{at}psu.edu; fax 814–863–1357.

Received December 14, 2004; returned for revision March 27, 2005; accepted March 27, 2005.




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