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Entry URI http://metadb.riken.jp/db/SciNetS_ria224i/cria224u4ria224u15923332i
Entry name Li Wuxing et al. 2005 Jun. Plant Physiol. 138(2):965-76.
Title The AtRAD51C gene is required for normal meiotic chromosome synapsis and double-stranded break repair in Arabidopsis.
Authors Li Wuxing|Lin Zhenguo|Ma Hong|Makaroff Christopher A|Timofejeva Ljudmilla|Xiao Rong|Yang Xiaohui
Abstract 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.
Pubmed ID 15923332
Journal Plant physiology
Volume 138
Issue 2
Pages 965-76
Publication date 2005 Jun
Num of phenotype gene 0