Participation of recombination proteins in rescue of arrested replication forks in UV-irradiated Escherichia coli need not involve recombination

Citation
J. Courcelle et Pc. Hanawalt, Participation of recombination proteins in rescue of arrested replication forks in UV-irradiated Escherichia coli need not involve recombination, P NAS US, 98(15), 2001, pp. 8196-8202
Citations number
62
Categorie Soggetti
Multidisciplinary
Journal title
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
ISSN journal
00278424 → ACNP
Volume
98
Issue
15
Year of publication
2001
Pages
8196 - 8202
Database
ISI
SICI code
0027-8424(20010717)98:15<8196:PORPIR>2.0.ZU;2-S
Abstract
Alternative reproductive cycles make use of different strategies to generat e different reproductive products. In Escherichia coli, recA and several ot her rec genes are required for the generation of recombinant genomes during Hfr conjugation. During normal asexual reproduction, many of these same ge nes are needed to generate clonal products from UV-irradiated cells. Howeve r, unlike conjugation, this latter process also requires the function of th e nucleotide excision repair genes. Following UV irradiation, the recovery of DNA replication requires uvrA and uvrC, as well as recA, recF, and recR. The rec genes appear to be required to protect and maintain replication fo rks that are arrested at DNA lesions, based on the extensive degradation of the nascent DNA that occurs in their absence. The products of the red and recQ genes process the blocked replication forks before the resumption of r eplication and may affect the fidelity of the recovery process. We discuss a model in which several rec gene products process replication forks arrest ed by DNA damage to facilitate the repair of the blocking DNA lesions by nu cleotide excision repair, thereby allowing processive replication to resume with no need for strand exchanges or recombination. The poor survival of c ellular populations that depend on recombinational pathways (compared with that in their excision repair proficient counterparts) suggests that at lea st some of the rec genes may be designed to function together with nucleoti de excision repair in a common and predominant pathway by which cells faith fully recover replication and survive following UV-induced DNA damage.