Ataxia telangiectasia mutated (ATM) has been known for decades as the main kinase mediating the DNA double-strand break response. Our recent findings suggest that its major role at the sites of breaks likely resides in its ability to modify both the local chromatin landscape and the global chromosome organization in order to promote repair accuracy.
Keywords: ATM; DNA double-strand break; chromatin; clustering; cohesin; topologically associated domains; γH2AX.