Disease relevance of recG

• A gene is identified in the Escherichia coli K-12 spo operon as recG [1].
• Effect of host species on recG phenotypes in Helicobacter pylori and Escherichia coli [2].

High impact information on recG

• The product of the recG gene of Escherichia coli is needed for normal recombination and DNA repair in E. coli and has been shown to help process Holliday junction intermediates to mature products by catalysing branch migration [3].
• Mutations in priA and recG increased or decreased deletion rates, but repeats were still greatly stabilized in the chromosome [4].
• The hbs4755 mutation did not modify the sensitivity of recH and addAB cells to the DNA-damaging agents methylmethane sulphonate (MMS) or 4-nitroquinoline-1-oxide (4NQO), and it only marginally affected recF and recG cells [5].
• A plasmid carrying the intact mmsA coding region was shown to restore UV resistance to E. coli recG mutant strains [6].
• The fact that in E. coli recG phenotypes are not constant in other species indicates the diverse roles for conserved recombination genes in prokaryotic evolution [2].

Biological context of recG

• Strains carrying null mutations in recG show reduced recombination and DNA repair [7].
• The mutant proteins retain the ability to catalyze primosome assembly, as judged by the viability of recG srgA and srgA strains and their ability to support replication of plasmids based on the ColE1 replicon [7].
• The nucleotide sequence of recG, the distal spo operon gene in Escherichia coli K-12 [1].
• The rap gene of bacteriophage lambda was placed in the chromosome of an Escherichia coli K-12 strain in which the recBCD gene cluster had previously been replaced by the lambda red genes and in which the recG gene had been deleted [8].
• To gain insight regarding the mechanisms that extend heteroduplex joints in Escherichia coli recombination, we investigated the effect of recG and ruv genotypes on heteroduplex strand polarity in intramolecular recombination products [9].

Other interactions of recG

• In contrast, frequencies of RecET-mediated illegitimate recombination were not affected by ruvAB, ruvC, recG, and recN mutations [10].
• A radA mutation was strongly synergistic with the recG Holliday junction helicase mutation, producing profound sensitivity to all DNA-damaging agents tested [11].
• (CAG)n.(CTG)n deletion rates were decreased, relative to the rates in wild type cells, in strains containing mutations in priA, recG, ruvAB, and recO [12].
• A mutation in the sfiA gene, which encodes and SOS-inducible inhibitor of septum formation, partially suppressed filamentation of recG mutant cells, but did not prevent the formation of anucleate cells [13].

References