Abstract
RAD51C is one of the RAD51 paralogs that plays an important role in DNA double-strand break repair by homologous recombination. Here, we identified and characterized OsRAD51C, the rice homolog of human RAD51C. The Osrad51c mutant plant is normal in vegetative growth but exhibits complete male and female sterility. Cytological investigation revealed that homologous pairing and synapsis were severely disrupted. Massive chromosome fragmentation occurred during metaphase I in Osrad51c meiocytes, and was fully suppressed by the CRC1 mutation. Immunofluorescence analysis showed that OsRAD51C localized onto the chromosomes from leptotene to early pachytene during prophase I, and that normal loading of OsRAD51C was dependent on OsREC8, PAIR2, and PAIR3. Additionally, ZEP1 did not localize properly in Osrad51c, indicating that OsRAD51C is required for synaptonemal complex assembly. Our study also provided evidence in support of a functional divergence in RAD51C among organisms.
Highlights
The maintenance of genome stability is essential for cell and organism viability
The specific functions of OsRAD51C in meiotic recombination, its spatial and temporal expression pattern, and its relationships with other determinant proteins in meiosis remain obscure. We identified another Osrad51c mutant showing a similar phenotype to that reported by Kou et al By studying chromosome behavior in Osrad51c, we found that OsRAD51C is required for processing of double-strand breaks (DSBs), homologous pairing, and synaptonemal complex (SC) assembly
When pollinated with wild-type pollen, the mutant plants still did not produce any seeds, demonstrating that megaspore development was affected. These results suggest that the sterile phenotype in Osrad51c was caused by both male and female sterility
Summary
The maintenance of genome stability is essential for cell and organism viability Both environmental and endogenous DNA damaging agents, including ionizing radiation, chemicals, and spontaneous DNA breakage during DNA recombination and replication can cause DNA lesions (Ward, 1988; Friedberg et al, 1995; Olive, 1998; Flores-Rozas and Kolodner, 2000). NHEJ completes DSB repair by directly ligating the DNA break ends without using a homologous template. Due to this imprecise repair mechanism, inappropriate NHEJ is potentially mutagenic and can lead to chromosome anomalies (Lees-Miller and Meek, 2003; Lieber, 2008)
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