Genome-wide CRISPR-KO screen for RAD52 synthetic lethal interactors

Rad52 plays essential roles in several homology-driven DNA repair pathways, including single strand annealing, transcription-coupled homologous recombination, and mitotic DNA synthesis (MiDAS). Although Rad52 is not essential, Rad52 loss with disruption of either the breast cancer 1 (BRCA1) or breast cancer 2 (BRCA2) genes is synthetic lethal. Thus, Rad52 is an intriguing potential target for treatment of BRCA-deficient cancers. However, the full breadth of pathways and factors that create a state of Rad52-dependence when compromised are not understood, and the goal of this project is to address this gap in knowledge. The data in this project represent completed genome-wide CRISPR knock-out screens in Rad52 Knock-out (Rad52KO) cells vs. wild-type (Rad52WT) to identify factors that are synthetic lethal with Rad52 (defined here as loss of fitness) under both untreated (NT) and stress conditions (cisplatin (Pt) or ionizing radiation (IR) treatments).