Assessing the role of the SMC-5/6 complex in meiotic double strand DNA break repair
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Meiosis is the specialized cell division used to form haploid gametes. During meiosis, endogenous double strand DNA breaks (DSBs) are induced. A subset of these DSBs must be repaired as crossovers with the homologous chromosome to ensure proper chromosome segregation. Although repair is required for proper chromosome segregation, use of the homologs as a repair template for DSB repair is restricted to a specific time window during meiotic prophase I. DSBs incurred outside of this window must be repaired to ensure genomic integrity. Multiple lines of evidence have suggested that these homolog-independent repair events utilize the sister chromatid as a template in repairing DSBs. Utilizing Caenorhabidits elegans, the Libuda lab has developed a genetic assay for intersister repair, directly demonstrating the occurrence of intersister repair events during meiosis; however, the molecular mechanism of intersister repair remains unknown. Previous studies have implicated multiple proteins in promoting homolog-independent DNA repair during meiosis, including the structural maintenance of chromosomes (SMC) 5/6 complex. Utilizing this assay, I will determine whether the SMC-5/6 complex is required for intersister repair during meiosis. Specifically, I will place an smc-5 null mutation in the intersister repair assay and examine the frequency of intersister repair events at a specific locus in the genome. If SMC-5 is required for intersister repair, I expect to observe a lowered frequency or elimination of intersister repair events compared to wild type controls. Determining the precise role of smc-5 and other candidate genes in DSB repair will provide insight into the mechanisms underlying DNA repair decisions during meiosis.