Connecting DNA damage with splicing decisions

The goal of anti-cancer therapies is often to create sufficient DNA damage to overwhelm the repair machinery and promote apoptosis. Although DNA damage impacts splice site selection, our understanding of the molecular mechanisms involved is only emerging. We investigated how the anticancer and DNA damaging agent oxaliplatin affects the splicing of the Bcl-x, which produces splice variants with pro- and anti-apoptotic functions. DNA damage reconfigures the interactions of RNA binding proteins to implement splicing switches on Bcl-x and other genes involved in the DNA damage response.