Abstract
The mammalian BREAST CANCER 2 (BRCA2) gene is a tumor suppressor that plays a crucial role in DNA repair and homologous recombination (HR). Here, we report the identification and characterization of OsBRCA2, the rice orthologue of human BRCA2. Osbrca2 mutant plants exhibit normal vegetative growth but experience complete male and female sterility as a consequence of severe meiotic defects. Pairing, synapsis and recombination are impaired in osbrca2 male meiocytes, leading to chromosome entanglements and fragmentation. In the absence of OsBRCA2, localization to the meiotic chromosome axes of the strand-invasion proteins OsRAD51 and OsDMC1 is severely reduced and in vitro OsBRCA2 directly interacts with OsRAD51 and OsDMC1. These results indicate that OsBRCA2 is essential for facilitating the loading of OsRAD51 and OsDMC1 onto resected ends of programmed double-strand breaks (DSB) during meiosis to promote single-end invasions of homologous chromosomes and accurate recombination. In addition, treatment of osbrca2-1 seedlings with mitomycin C (MMC) led to hypersensitivity. As MMC is a genotoxic agent that creates DNA lesions in the somatic cells that can only be repaired by HR, these results suggest that OsBRCA2 has a conserved role in DSB repair and HR in rice.
Highlights
Cellular DNA of living organisms experience DNA damage caused by exogenous and endogenous factors
OsBRCA2 Is Indispensable for Homologous Chromosome Pairing, Synapsis and DNA Repair in Rice Meiosis
Orthologues of BREAST CANCER 2 (BRCA2) have been characterized in Arabidopsis (Siaud et al, 2004; Seeliger et al, 2012), it is yet unclear how widely these functions are conserved in other plants
Summary
Cellular DNA of living organisms experience DNA damage caused by exogenous and endogenous factors. DNA double-strand breaks (DSBs) are one of the most cytotoxic DNA lesions, as even one single unrepaired or misrepaired DSB will lead to genomic rearrangements and genome instability (Bennett et al, 1993; Sandell and Zakian, 1993). Non-homologous end joining (NHEJ) and homologous recombination (HR) are the two main pathways involved in the repair of DSBs (Bétermier et al, 2014; Guirouilh-Barbat et al, 2014). In the NHEJ pathway, DNA broken ends are repaired by rapidly ligating the two DNA ends with little to no DNA end processing. In addition to accidental mitotic DSBs, HR is indispensable for repairing programmed meiotic
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