Does the failure in innate immunity establish senescence? The c-Abl story

DNA damage response determines cell fate. A classical view is that under DNA damage cells either die or survive while maintaining a certain degree of genome instability and rearrangements. A significant number of these surviving cells harbor MNi. MNi has lately been reported to activate the cGAS-STING innate immunity pathway. Remarkably, the same cGAS-STING pathway plays a role in inducing senescence Our preliminary data suggest that under c-Abl inhibition/knockout the IFN-I pathway is compromised whereas the senescence program is activated. We will investigate the possibility that failure to activate innate immunity (IFN-I) facilitates senescence.