DNA damage foci in mitosis are devoid of 53BP1.

Nuclear DNA damage foci indicate ongoing DNA damage response, which is the major inducer of cell cycle arrest, cellular senescence and apoptosis. 53BP1 is one central mediator of the DNA damage response and a component of active DNA damage foci. Using an AcGFP-53BP1c fluorescent fusion protein that quantitatively reports DNA damage, we show that the recruitment of 53BP1 into gammaH2A.X-containing DNA damage foci was inhibited at G(2)/M. This suggests a possible mechanism for cells to continue through the G(2) checkpoint with gammaH2A.X-flagged double strand breaks via inhibition of 53BP1-mediated DNA damage signalling.