Genomic Stability Impact of Combined Xrcc4 and ATM Deficiency in B Cells
This summer, I participated in the CURE Program at Dana Farber / Harvard Cancer Center, where I studied the impact of Xrcc4 and ATM inactivation on mature B cells. B cells are essential components of our immune system that are involved in the eradication of pathogens from our body. These cells undergo a process of genetic recombination called Class Switching Recombination (CSR) after the encounter of pathogens, in order to bind different effector molecules. Class Switching Recombination results in double stranded breaks in B cells that are repaired by the Non-homologous End Joining (NHEJ) DNA repair pathway. I studied the effects of two important genes: XRCC4 and ATM on NHEJ DNA repair pathway during Class Switching Recombination of mature B cells. I used Fluorescent In Situ Hybridization (FISH) assay for my study, which is a technique that allows for the observation of DNA breaks, chromosomal breaks and translocations in the genome.