THE ROLE OF THE SUMO INTERACTING MOTIF IN DNA REPAIR AT DAMAGED REPLICATION FORKS BY BLM PROTEIN

Abstract

DNA repair is a crucial process in maintaining genomic stability and avoiding adverse effects on human health such as cancer. One important protein in DNA damage repair is BLM. In people with Bloom’s syndrome, the BLM gene, which encodes BLM protein, results in either catalytically inactive BLM or fails to produce detectable BLM protein at all. BLM is a RecQ helicase important for unwinding DNA at sites of DNA damage to regulate homologous recombination at stalled replication forks. There are important sites on the BLM protein for further regulating its function by allowing for post-translational modifications by Small Ubiquitin-like Modifier (SUMO). Specific sites on the BLM protein have been found to be important for modification by SUMO. These sites include a SUMO-acceptor (SM) site and SUMO interacting motif (SIM) site. SIM-BLM and SM-SIM-BLM plasmids were constructed, and BLM+ and SM-BLM stable cell lines were produced to further study the role of SUMO in the function of BLM.