A method was developed to examine DNA repair within the intact cell. U
ltrasoft x-rays were used to induce DNA double-strand breaks (DSBs) in
defined subnuclear volumes of human fibroblasts and DNA repair was vi
sualized at those sites. The DSBs remained in a fixed position during
the initial stages of DNA repair, and the DSB repair protein hMre11 mi
grated to the sites of damage within 30 minutes. In contrast, hRad51,
a human RecA homolog, did not localize at sites of DNA damage, a findi
ng consistent with the distinct roles of these proteins in DNA repair.