Main content area

TRF2 is required for repair of nontelomeric DNA double-strand breaks by homologous recombination

Mao, Zhiyong, Seluanov, Andrei, Jiang, Ying, Gorbunova, Vera
Proceedings of the National Academy of Sciences of the United States of America 2007 v.104 no.32 pp. 13068-13073
DNA, DNA damage, DNA repair, gamma radiation, homologous recombination, telomeres
TRF2 (telomeric repeat binding factor 2) is an essential component of the telomeric cap, where it forms and stabilizes the T-loop junctions. TRF2 forms the T-loops by stimulating strand invasion of the 3' overhang into duplex DNA. TRF2 also has been shown to localize to nontelomeric DNA double-strand breaks, but its functional role in DNA repair has not been examined. Here, we present evidence that TRF2 is involved in homologous recombination (HR) repair of nontelomeric double-strand breaks. Depletion of TRF2 strongly inhibited HR and delayed the formation of Rad51 foci after γ-irradiation, whereas overexpression of TRF2 stimulated HR. Depletion of TRF2 had no effect on nonhomologous end-joining, and overexpression of TRF2 inhibited nonhomologous end-joining. We propose, based on our results and on the ability of TRF2 to mediate strand invasion, that TRF2 plays an essential role in HR by facilitating the formation of early recombination intermediates.