Gap formation is associated with methyl-directed mismatch correction under conditions of restricted DNA synthesis

Genome ◽  
1989 ◽  
Vol 31 (1) ◽  
pp. 104-111 ◽  
Author(s):  
Shin-San Su ◽  
Michelle Grilley ◽  
Randy Thresher ◽  
Jack Griffith ◽  
Paul Modrich
Keyword(s):  
Escherichia Coli ◽  
Dna Repair ◽  
Dna Synthesis ◽  
Gene Conversion ◽  
Strand Displacement ◽  
Gap Formation ◽  
Repair Gene ◽  
Mismatch Correction ◽  
Dna Repair Gene ◽  
Gatc Site

A covalently closed, circular heteroduplex containing a G – T mismatch and a single hemimethylated d(GATC) site is subject to efficient methyl-directed mismatch correction in Escherichia coli extracts when repair DNA synthesis is severely restricted by limiting the concentration of exogenously supplied deoxyribonucleoside-5′-triphosphates or by supplementing reactions with chain-terminating 2′,3′-dideoxynucleoside triphosphates. However, repair under these conditions results in formation of a single-strand gap in the region of the molecule containing the mismatch and the d(GATC) site. These findings indicate that repair DNA synthesis required for methyl-directed correction can initiate in the vicinity of the mispair, and they are most consistent with a repair reaction involving 3′ → 5′ excision (or strand displacement) from the d(GATC) site followed by 5′ → 3′ repair DNA synthesis initiating in the vicinity of the mismatch.Key words: DNA repair, gene conversion, mismatch correction, mutagenesis.

scholarly journals Error-Prone DNA Repair System in Enteroaggregative Escherichia coli Identified by Subtractive Hybridization

2007 ◽  
Vol 189 (10) ◽  
pp. 3793-3803 ◽  
Author(s):  
Lucy M. Joo ◽  
Louissa R. Macfarlane-Smith ◽  
Iruka N. Okeke
Keyword(s):  
Escherichia Coli ◽  
Dna Repair ◽  
Subtractive Hybridization ◽  
Repair System ◽  
Repair Gene ◽  
E Coli ◽  
Eaec Strain ◽  
Etiologic Agents ◽  
Dna Repair Gene ◽  
Error Prone Repair

ABSTRACT Enteroaggregative Escherichia coli (EAEC) are etiologic agents of diarrhea. The EAEC category is heterogeneous, but most in-depth experimentation has focused on prototypical strain, 042. We hypothesized that 60A, another EAEC strain, might posses virulence or fitness genes that 042 does not have. Through subtractive hybridization we identified 60A-specific sequences, including loci present in other E. coli and phage DNA. One locus thus identified was impB, a LexA repressed error-prone DNA repair gene that has been identified in plasmids from other enteric organisms and which we detected in 21 of 34 EAEC strains. An isogenic 60A impB mutant showed decreased survival and mutagenesis after exposure to UV, as well as bile salt exposure, compared to the wild-type strain, and these phenotypes could be complemented in trans. The EAEC strain 60A imp operon differs structurally from previously described homologs. A cryptic gene, impC, present in other imp operons, is absent from 60A. In addition, transcription of impAB in strain 60A occurs from a promoter that is dissimilar to the previously described impC promoter but is still triggered by UV-mediated damage. In strain 60A the impAB and the aggregative adherence fimbriae I (AAF/I)-encoding genes are on the same large plasmid, and the 60A version of the operon is predominantly seen in AAF/I-positive EAEC. Supplementary imp SOS-inducible error-prone repair systems are common among EAEC even though they are absent in prototypical strain 042.

scholarly journals XRS2, a DNA repair gene of Saccharomyces cerevisiae, is needed for meiotic recombination.

Genetics ◽  
1992 ◽  
Vol 132 (3) ◽  
pp. 651-664 ◽  
Author(s):  
E L Ivanov ◽  
V G Korolev ◽  
F Fabre
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Gene Conversion ◽  
Meiotic Recombination ◽  
Repair Gene ◽  
Strand Breaks ◽  
Dna Repair Gene ◽  
Mating Type Switching ◽  
Radiation Induced ◽  
Recombination Pathway

Abstract The XRS2 gene of Saccharomyces cerevisiae has been previously identified as a DNA repair gene. In this communication, we show that XRS2 also encodes an essential meiotic function. Spore inviability of xrs2 strains is rescued by a spo13 mutation, but meiotic recombination (both gene conversion and crossing over) is highly depressed in spo13 xrs2 diploids. The xrs2 mutation suppresses spore inviability of a spo13 rad52 strain suggesting that XRS2 acts prior to RAD52 in the meiotic recombination pathway. In agreement with the genetic data, meiosis-specific double-strand breaks at the ARG4 meiotic recombination hotspot are not detected in xrs2 strains. Despite its effects on meiotic recombination, the xrs2 mutation does not prevent mitotic recombination events, including homologous integration of linear DNA, mating-type switching and radiation-induced gene conversion. Moreover, xrs2 strains display a mitotic hyper-rec phenotype. Haploid xrs2 cells fail to carry out G2-repair of gamma-induced lesions, whereas xrs2 diploids are able to perform some diploid-specific repair of these lesions. Meiotic and mitotic phenotypes of xrs2 cells are very similar to those of rad50 cells suggesting that XRS2 is involved in homologous recombination in a way analogous to that of RAD50.

scholarly journals Characterization of dinY, a new Escherichia coli DNA repair gene whose products are damage inducible even in a lexA(Def) background.

1993 ◽  
Vol 175 (3) ◽  
pp. 642-646 ◽  
Author(s):  
C Petit ◽  
C Cayrol ◽  
C Lesca ◽  
P Kaiser ◽  
C Thompson ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Dna Repair ◽  
Repair Gene ◽  
Dna Repair Gene

Repair of base–base mismatches in simian and human cells

Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 578-583 ◽  
Author(s):  
Thomas C. Brown ◽  
Josef Jiricny
Keyword(s):  
Dna Methylation ◽  
Dna Repair ◽  
Gene Conversion ◽  
Human Fibroblasts ◽  
Repair Gene ◽  
Dna Repair Gene ◽  
Flanking Sequences ◽  
Sv40 Dna ◽  
Derivatives Of ◽  
Genetic Events

Mismatched heteroduplexes arise as intermediates of several dissimilar genetic processes. The outcome of these genetic events will therefore be influenced by the efficiency and specificity of mismatch repair. We have studied the correction of base–base mispairs in simian and human fibroblasts by transfecting the cells with derivatives of SV40 DNA, each harboring a single mispair in a defined orientation. Analysis of plaques revealed that correction efficiencies for homomispairs followed the pattern G∙G > C∙C ≥ A∙A > T∙T. Repair bias was influenced by flanking sequences. Correction efficiencies for heteromispairs followed the pattern of G∙T > A∙C > C∙T > A∙G and repair favored the retention of G+C by a substantial margin. This repair specificity could lead to a gene conversion bias favoring the accumulation of G+C in sequences subject to high levels of recombination or unequal exchange.Key words: DNA repair, gene conversion, recombination, DNA methylation.

scholarly journals The Saccharomyces cerevisiae RAD30 Gene, a Homologue of Escherichia coli dinB and umuC, Is DNA Damage Inducible and Functions in a Novel Error-Free Postreplication Repair Mechanism

Genetics ◽  
1997 ◽  
Vol 147 (4) ◽  
pp. 1557-1568 ◽  
Author(s):  
John P McDonald ◽  
Arthur S Levine ◽  
Roger Woodgate
Keyword(s):  
Escherichia Coli ◽  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Uv Resistance ◽  
Repair Mechanism ◽  
Repair Gene ◽  
Epistasis Analysis ◽  
Dna Repair Gene ◽  
Induced Mutagenesis

Abstract Damage-inducible mutagenesis in prokaryotes is largely dependent upon the activity of the UmuD'C like proteins. Since many DNA repair processes are structurally and/or functionally conserved between prokaryotes and eukaryotes, we investigated the role of RAD30 a previously uncharacterized Saccharomyces cerevisiae DNA repair gene related to the Escherichia coli dinB, umuC and S. cerevisiae REV1 genes, in UV resistance and UV-induced mutagenesis. Similar to its prokaryotic homologues, RAD30 was found to be damage inducible. Like many S. cerevisiae genes involved in error-prone DNA repair, epistasis analysis clearly places RAD30 in the RAD6 group and rad30 mutants display moderate UV sensitivity reminiscent of rev mutants. However, unlike rev mutants, no defect in UV-induced reversion was seen in rad30 strains. While rad6 and rad18 are both epistatic to rad30, no epistasis was observed with rev1, rev3, rev7 or rad5, all of which are members of the RAD6 epistasis group. These findings suggest that RAD30 participates in a novel error-free repair pathway dependent on RAD6 and RADl8, but independent of REV1, REV3, REV7 and RAD5.

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