FAM72A promotes mutagenic repair during antibody maturation

Genome-wide CRISPR screen in murine CH12F3-2 cell line to identify novel factors involved in antibody class switch recombination. FAM72A, a protein with no ascribed function, was identified in this screen as a major determinant during mutagenic uracil repair by antagonizing base excision repair protein UNG2. Overall design: CH12F3-2 cells were transduced with the CRISPR gRNA library, followed by C.I.T cocktail treatment to allow antibody class switching to occur from IgM to IgA. Cells were stained for surface IgA expression and FACS sorting was done to separate IgA+ population from IgA- population. gRNA representation was compared from IgA+ or IgA- population to the unsorted to determine genes involved in CSR.