Damage to DNA induces expression of the ruv gene of Escherichia coli

Shurvinton, Claire E.; Lloyd, Robert G.

doi:10.1007/bf00330811

Cited by 101 publications

(64 citation statements)

References 24 publications

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“…Because this test can only be used for values Ն 5, the hypergeometric law was used for the uvrD ::Tn5 ⌬(recA-srl )::Tn10 and the lexA ind3 strains for which the set was too small. (Shurvington and Lloyd, 1982;Shinagawa et al, 1988) and catalyse branch migration of Holliday junctions before resolution (Rafferty et al, 1996;Yu et al, 1997;Eggleston et al, 1997). The effect of a ruvA::Tn10 mutation, which abolishes the SOS-induced pathway of Holliday junction resolution, was therefore tested in uvrD mutants.…”

Section: Isolation Of Mutants With Increased Deletion Ratesmentioning

confidence: 99%

“…Because some of the genes involved in the recF recombination pathway, such as recN (Finch et al, 1985), recQ (Irino et al, 1986) and ruvA (Shurvington and Lloyd, 1982), are under the control of LexA, we examined the possible involvement of this pathway in uvrD-stimulated TRD. The RecF, RuvAB and RecQ proteins are required for more than 90% of the deletion events in uvrD mutants.…”

Section: Recf-dependent Pathway For Uvrd-stimulated Recombinationmentioning

confidence: 99%

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uvrD mutations enhance tandem repeat deletion in the Escherichia coli chromosome via SOS induction of the RecF recombination pathway

Bierne

Seigneur

et al. 1997

Molecular Microbiology

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SummaryIt has previously been shown that recombination between tandem repeats is not significantly affected by a recA mutation in Escherichia coli. Here, we describe the activation of a RecA-dependent recombination pathway in a hyper-recombination mutant. In order to analyse how tandem repeat deletion may proceed, we searched for mutants that affect this process. Three hyper-recombination clones were characterized and shown to be mutated in the uvrD gene. Two of the mutations were identified as opal mutations at codons 130 and 438. A uvrD ::Tn5 mutation was used to investigate the mechanism of deletion formation in these mutants. The uvrD-mediated stimulation of deletion was abolished by a lexAind3 mutation or by inactivation of either the recA, recF, recQ or ruvA genes. We conclude that (i) this stimulation requires SOS induction and (ii) tandem repeat recombination in uvrD mutants occurs via the RecF pathway. In uvrD þ cells, constitutive expression of SOS genes is not sufficient to stimulate deletion formation. This suggests that the RecF recombination pathway activated by SOS induction is antagonized by the UvrD protein. Paradoxically, we observed that the overproduction of UvrD from a plasmid also stimulates tandem repeat deletion. However, this stimulation is RecA independent, as is deletion in a wild-type strain. We propose that the presence of an excess of the UvrD helicase favours replication slippage. This work suggests that the UvrD helicase controls a balance between different routes of tandem repeat deletion.

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Section: Isolation Of Mutants With Increased Deletion Ratesmentioning

confidence: 99%

Section: Recf-dependent Pathway For Uvrd-stimulated Recombinationmentioning

confidence: 99%

uvrD mutations enhance tandem repeat deletion in the Escherichia coli chromosome via SOS induction of the RecF recombination pathway

Bierne

Seigneur

et al. 1997

Molecular Microbiology

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“…Although ruv mutations have little effect on conjugal recombination in otherwise wild-type strains, they reduce the ability of recombination in recBC sbcA and recBC sbcBC strains (11)(12)(13). This evidence suggests that the ruv locus may be involved in recombinational repair by the RecE and the RecF pathways.The ruv locus contains two genes, ruvA and ruvB, that constitute an operon regulated by the SOS system (3,27,29). Recently these genes were also shown to be involved in mutagenesis induced by UV and X irradiation and by some chemicals (9, 24).…”

mentioning

confidence: 99%

“…The ruv locus contains two genes, ruvA and ruvB, that constitute an operon regulated by the SOS system (3,27,29). Recently these genes were also shown to be involved in mutagenesis induced by UV and X irradiation and by some chemicals (9,24).…”

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confidence: 99%

Molecular analysis of the Escherichia coli ruvC gene, which encodes a Holliday junction-specific endonuclease

et al. 1991

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The Escherichia coli ruvC gene is involved in DNA repair and recombination and encodes an endonuclease that resolves Holliday structure in vitro. The 2.8-kb chromosomal DNA fragment that encompasses the ruvC gene and its flanking regions was cloned and sequenced. Four open reading frames were identified in the order orfl7-orJ26-ruvC-orfJ3 immediately upstream of the ruvAB operon, and their orientations are the same as the ruvAB operon, except for orf23. Proteins encoded by orfl7, or426, and ruvC (orfl9) were identified by the maxicell method, and their sizes agreed with those predicted from the DNA sequences. Among the open reading frames in this region, only ruvC is involved in the repair of UV-damaged DNA. ruvC appeared to be regulated by at least two promoters, but, in contrast to the ruvAB operon, ruvC is not regulated by the SOS system as demonstrated by operon fusions.Escherichia coli strains carrying mutations in the ruv locus were isolated initially as mutants which were sensitive to mitomycin C (19) or which showed reduced ability of recombination between duplicated gal genes (32). These mutants are also sensitive to various DNA-damaging agents such as UV, ionizing radiation, and some chemical mutagens, and they form multinucleated cells after treatment with low doses of such agents (18)(19)(20)32). Although ruv mutations have little effect on conjugal recombination in otherwise wild-type strains, they reduce the ability of recombination in recBC sbcA and recBC sbcBC strains (11)(12)(13). This evidence suggests that the ruv locus may be involved in recombinational repair by the RecE and the RecF pathways.The ruv locus contains two genes, ruvA and ruvB, that constitute an operon regulated by the SOS system (3,27,29). Recently these genes were also shown to be involved in mutagenesis induced by UV and X irradiation and by some chemicals (9, 24). The purified RuvB protein possesses weak ATPase activity (7), which is stimulated by the RuvA protein in the presence of DNA (26). The RuvA-RuvB complex in the presence of ATP renatures cruciform structure in supercoiled DNA with a palindromic sequence, indicating that it may promote strand exchange reactions in homologous recombination (26).While we were cloning the chromosomal DNA fragment that complemented the repair defect in the ruv mutants, we noticed that the phenotype of one of the ruv mutants we analyzed, CS85 (ruv-53), was not complemented by the plasmid carrying the ruvAB operon, but was complemented by the chromosomal DNA region upstream of the ruvAB operon. Sharples et al. (25) have identified the approximate location of this mutation on the physical map of this region and designated it ruvC. The ruvC mutants, as with the other ruv mutants, are defective in DNA repair and recombination of the RecE and the RecF pathways (1,12,19,25,30). In this study we analyzed the nucleotide sequence of the ruvC gene and its flanking regions and identified the proteins encoded by the ruvC region.RuvC protein has been highly purified recently and has an * Correspondin...

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“…Our previous study shows that RecG is present at ϳ3 molecules in M. tuberculosis cells, and its level marginally increases with DNA damage (53). In contrast to RecG, the basal levels of E. coli RuvA and RuvB proteins are known to exist at ϳ700 and 200 molecules, respectively (75,76). E. coli RuvA assembles into a tetramer, whereas RuvB exists as hexamer and such oligomeric forms of RuvA/RuvB are required for its optimal activity to catalyze unwinding of HJ as well as fork structures (21,(77)(78)(79).…”

Section: Discussionmentioning

confidence: 99%

Mycobacterium tuberculosis RecG Protein but Not RuvAB or RecA Protein Is Efficient at Remodeling the Stalled Replication Forks

Thakur¹,

Basavaraju²,

Khanduja³

et al. 2015

Journal of Biological Chemistry

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Damage to DNA induces expression of the ruv gene of Escherichia coli

Cited by 101 publications

References 24 publications

uvrD mutations enhance tandem repeat deletion in the Escherichia coli chromosome via SOS induction of the RecF recombination pathway

uvrD mutations enhance tandem repeat deletion in the Escherichia coli chromosome via SOS induction of the RecF recombination pathway

Molecular analysis of the Escherichia coli ruvC gene, which encodes a Holliday junction-specific endonuclease

Mycobacterium tuberculosis RecG Protein but Not RuvAB or RecA Protein Is Efficient at Remodeling the Stalled Replication Forks

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