Cell-cycle-regulated association of RAD50/MRE11/NBS1 with TRF2 and human telomeres.

摘要: Telomeres allow cells to distinguish natural chromosome ends from damaged DNA and protect the degradation fusion. In human cells, telomere protection depends on TTAGGG repeat binding factor, TRF2 (refs 1–4), which has been proposed remodel telomeres into large duplex loops5 (t-loops). Here we show by nanoelectrospray tandem mass spectrometry that RAD50 protein is present in immunocomplexes. Protein blotting showed a small fraction of RAD50, MRE11 third component double-strand break (DSB) repair complex, Nijmegen breakage syndrome (NBS1), associated with TRF2. Indirect immunofluorescence demonstrated presence at interphase telomeres. NBS1 was S phase, but not G1 or G2. Although complex accumulated irradiation-induced foci (IRIFs) response γ-irradiation, did relocate IRIFs irradiation affect association arguing against role for DSB repair. Instead, propose functions telomeres, possibly modulating t-loop formation.