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Multiple mechanisms control chromosome integrity after replication fork uncoupling and restart at irreparable UV lesions.

Abstract：

:DNA replication forks pause in front of lesions on the template, eventually leading to cytotoxic chromosomal rearrangements. The in vivo structure of damaged eukaryotic replication intermediates has been so far elusive. Combining electron microscopy (EM) and two-dimensional (2D) gel electrophoresis, we found that UV-irradiated S. cerevisiae cells uncouple leading and lagging strand replication at irreparable UV lesions, thus generating long ssDNA regions on one side of the fork. Furthermore, small ssDNA gaps accumulate along replicated duplexes, likely resulting from repriming events downstream of the lesions on both leading and lagging strands. Translesion synthesis and homologous recombination counteract gap accumulation, without affecting fork progression. The DNA damage checkpoint contributes to gap repair and maintains a replication-competent fork structure. We propose that the coordinated action of checkpoint, recombination, and translesion synthesis-mediated processes at the fork and behind the fork preserves the integrity of replicating chromosomes by allowing efficient replication restart and filling the resulting ssDNA gaps.

journal_name

Mol Cell

journal_title

Molecular cell

authors

Lopes M,Foiani M,Sogo JM

doi

10.1016/j.molcel.2005.11.015

subject

Has Abstract

pub_date

2006-01-06 00:00:00

pages

15-27

issue

1

eissn

1097-2765

issn

1097-4164

pii

S1097-2765(05)01802-2

journal_volume

21

pub_type

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