Practice question

DNA double strand breaks immediately trigger checkpoint kinases ATM and DNA-PK. Histone variant H2A.X widely replacing small fraction of H2A throughout genome becomes rapidly phosphorylated at serine 139 over domains extending megabases surrounding breaks, forming gamma-H2A.X foci detectable by immunofluorescence. Phosphorylated tail recruits mediator MDC1, ubiquitin ligases RNF8, 53BP1 and BRCA1 complexes promoting nonhomologous end joining and homologous recombination repair pathway choice. CENP-A marks centromere epigenetically, H2A.Z regulates promoter activity, H3.3 deposited at active genes. Gamma-H2A.X serves as sensitive biomarker for damage quantitation used clinically.