Linked Life Data

19017273

Source:http://linkedlifedata.com/resource/pubmed/id/19017273

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-1-23
pubmed:abstractText
In Escherichia coli, RecF-dependent post-replication repair (PRR) permits cells to tolerate the potentially lethal effects of blocking lesions at the replication fork. We have developed an in vivo experimental system to study the PRR mechanisms that allow blocked replication forks to be rescued by homologous sequences. We show that approximately 80% of the PRR events observed in SOS-uninduced cells are generated by RecA-mediated excision repair, a novel nucleotide excision repair- and RecA/RecF-dependent mechanism, while 20% are generated by RecF-dependent homologous recombination. Moreover, we show that in a wild-type background, PRR is approximately an order of magnitude more efficient in processing DNA containing a blocked leading strand, as compared with a blocked lagging strand. This strand bias is abolished in cells that are deficient in nucleotide excision repair. These results are discussed in the context of recent models describing the mechanisms of replication past damaged templates.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1365-2958
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
71
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
305-14
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Preferential post-replication repair of DNA lesions situated on the leading strand of plasmids in Escherichia coli.
pubmed:affiliation
Université Strasbourg 1, Institut Gillbert Laustrait, CNRS-UMR 7175. Boulevard Sebastien Brant, BP 10413, F-67412 Illkirch-Cedex, France. bichara@esbs.u-strasbg.fr
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't