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.

Increased resistance to the toxic effects of alkylating agents in tobacco expressing the E. coli DNA repair gene ada

1992 ◽  
Vol 273 (3) ◽  
pp. 271-280 ◽  
Author(s):  
K. Angelis ◽  
J. Bříza ◽  
J. Šatava ◽  
I. Skákal ◽  
J. Velemínský ◽  
...  
Keyword(s):  
Dna Repair ◽  
Alkylating Agents ◽  
Toxic Effects ◽  
Repair Gene ◽  
E Coli ◽  
Dna Repair Gene

scholarly journals Lasting DNA Damage and Aberrant DNA Repair Gene Expression Profile Are Associated with Post-Chronic Cadmium Exposure in Human Bronchial Epithelial Cells

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 842 ◽  
Author(s):  
Heng Wee Tan ◽  
Zhan-Ling Liang ◽  
Yue Yao ◽  
Dan-Dan Wu ◽  
Hai-Ying Mo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Damage ◽  
Dna Repair ◽  
Human Lung ◽  
Repair System ◽  
Dna Repair Genes ◽  
Repair Gene ◽  
Dna Repair Gene ◽  
Repair Genes ◽  
Cd Exposure

Cadmium (Cd) is a widespread environmental pollutant and carcinogen. Although the exact mechanisms of Cd-induced carcinogenesis remain unclear, previous acute/chronic Cd exposure studies have shown that Cd exerts its cytotoxic and carcinogenic effects through multiple mechanisms, including interference with the DNA repair system. However, the effects of post-chronic Cd exposure remain unknown. Here, we establish a unique post-chronic Cd-exposed human lung cell model (the “CR0” cells) and investigate the effects of post-chronic Cd exposure on the DNA repair system. We found that the CR0 cells retained Cd-resistant property even though it was grown in Cd-free culture medium for over a year. The CR0 cells had lasting DNA damage due to reduced DNA repair capacity and an aberrant DNA repair gene expression profile. A total of 12 DNA repair genes associated with post-chronic Cd exposure were identified, and they could be potential biomarkers for identifying post-chronic Cd exposure. Clinical database analysis suggests that some of the DNA repair genes play a role in lung cancer patients with different smoking histories. Generally, CR0 cells were more sensitive to chemotherapeutic (cisplatin, gemcitabine, and vinorelbine tartrate) and DNA damaging (H2O2) agents, which may represent a double-edged sword for cancer prevention and treatment. Overall, we demonstrated for the first time that the effects of post-chronic Cd exposure on human lung cells are long-lasting and different from that of acute and chronic exposures. Findings from our study unveiled a new perspective on Cd-induced carcinogenesis—the post-chronic exposure of Cd. This study encourages the field of post-exposure research which is crucial but has long been ignored.

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 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

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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