Presenter(s): Rachel David − Biochemistry
Faculty Mentor(s): Diana Libuda, Erik Toraason
Oral Session 3M
Research Area: Biological Sciences
Funding: UO Alden Scholar Research Award, NICHD Grant
During meiosis, the specialized form of cell division that produces gametes, cells utilize recombination to maintain genomic integrity and promote proper chromosome segregation, ensuring fertility. Double-strand DNA breaks (DSBs), which serve as substrates for homologous recombination, are intentionally induced during meiosis. A fraction of DSBs must be repaired
as crossover recombination events with the homologous chromosome to forge a physical connection required to facilitate proper chromosome segregation. Although DSBs are induced across the genome, crossovers in C. elegans are preferentially formed along chromosome arms and not the center of chromosomes. What determines this crossover preference along chromosome arms is not well known. Intriguingly, previous studies in C. elegans have indicated that the crossover landscape is not determined by chromatin marks or specific sequence motifs. However, proximity of a DSB to the synaptonemal complex (SC), a meiosis-specific proteinaceous structure that connects homologous chromosomes together, has been suggested to influence DSB repair outcomes. To determine how genomic positioning of a DSB affects its repair outcome, I am exploiting genetic assays developed by the Libuda lab that enable controlled induction of a single DSB at a known genomic location and assess how that induced DSB was repaired. Utilizing CRISPR/Cas9 genome editing, I have targeted these assays to four unique loci that differ in position both along the chromosome length and in proximity to the SC. Together, our studies will elucidate how the position of a DSB within the genome influences how it is repaired to maintain genome integrity.