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PubMed · 12543983

DNA damage-induced replication fork regression and processing in Escherichia coli.

Justin Courcelle·Janet R Donaldson·Kin-Hoe Chow·Charmain T Courcelle
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Abstract

DNA lesions that block replication are a primary cause of rearrangements, mutations, and lethality in all cells. After ultraviolet (UV)-induced DNA damage in Escherichia coli, replication recovery requires RecA and several other recF pathway proteins. To characterize the mechanism by which lesion-blocked replication forks recover, we used two-dimensional agarose gel electrophoresis to show that replication-blocking DNA lesions induce a transient reversal of the replication fork in vivo. The reversed replication fork intermediate is stabilized by RecA and RecF and is degraded by the RecQ-RecJ helicase-nuclease when these proteins are absent. We propose that fork regression allows repair enzymes to gain access to the replication-blocking lesion, allowing processive replication to resume once the blocking lesion is removed.

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Adenosine TriphosphatasesBacterial ProteinsDNA DamageDNA HelicasesDNA RepairDNA ReplicationDNA, BacterialDNA-Binding ProteinsElectrophoresis, Agar GelElectrophoresis, Gel, Two-DimensionalEscherichia coliEscherichia coli ProteinsExodeoxyribonucleasesNucleic Acid ConformationPlasmidsRec A RecombinasesRecQ HelicasesUltraviolet RaysJournal ArticleResearch Support, U.S. Gov't, Non-P.H.S.

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Justin Courcelle, Janet R Donaldson, Kin-Hoe Chow, Charmain T Courcelle. 2003-01-23. DNA damage-induced replication fork regression and processing in Escherichia coli.. https://doi.org/10.1126/science.1081328

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