Human SNM1B/Apollo is involved in the cellular response to DNA-damage, however, its
precise role is unknown. Recent reports have implicated hSNM1B in the protection of
telomeres. We have found hSNM1B to interact with TRF2, a protein which functions in
telomere protection and in an early response to ionizing radiation. Here we show that
endogenous hSNM1B forms foci which colocalize at telomeres with TRF1 and TRF2. However,
we observed that additional hSNM1B foci could be induced upon exposure to ionizing
radiation (IR). In live-cell-imaging experiments, hSNM1B localized to photo-induced
double-strand breaks (DSBs) within 10s post-induction. Further supporting a role for
hSNM1B in the early stages of the cellular response to DSBs, we observed that autophosphorylation
of ATM, as well as the phosphorylation of ATM target proteins in response to IR, was
attenuated in cells depleted of hSNM1B. These observations suggest an important role
for hSNM1B in the response to IR damage, a role that may be, in part, upstream of
the central player in maintenance of genome integrity, ATM.