A RAP1/TRF2 complex inhibits nonhomologous end-joining at human telomeric DNA ends.

Abstract:

:The mechanisms by which telomeres are distinguished from DNA double-strand breaks are poorly understood. Here we have defined the minimal requirements for the protection of telomeric DNA ends from nonhomologous end-joining (NHEJ). Neither long, single-stranded overhangs nor t loop formation is essential to prevent NHEJ-mediated ligation of telomeric ends in vitro. Instead, a tandem array of 12 telomeric repeats is sufficient to impede illegitimate repair in a highly directional manner at nearby DNA ends. The polarity of end protection is consistent with the orientation of naturally occurring telomeres and is well suited to minimize interference between chromosome capping and the repair of DNA double-strand breaks in subtelomeric sequences. Biochemical fractionation and reconstitution revealed that telomere protection is mediated by a RAP1/TRF2 complex, providing evidence for a direct role for human RAP1 in the protection of telomeric DNA from NHEJ.

journal_name

Mol Cell

journal_title

Molecular cell

authors

Bae NS,Baumann P

doi

10.1016/j.molcel.2007.03.023

subject

Has Abstract

pub_date

2007-05-11 00:00:00

pages

323-34

issue

3

eissn

1097-2765

issn

1097-4164

pii

S1097-2765(07)00214-6

journal_volume

26

pub_type

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