The ATM-BID pathway regulates quiescence and survival of haematopoietic stem cells.

The ATM motif was previously shown to phosphorylate the BH3-only BID protein, a pro-apoptotic member of the BCL2 family. Using transgenic mice expressing a phosphodefective BID, Gross and colleagues find that the ATM effect on BID prevents its translocation to the mitochondria, where the effects of BID on ROS would trigger haematopoietic stem cells to exit quiescence.