Document Detail


RdgB acts to avoid chromosome fragmentation in Escherichia coli.
MedLine Citation:
PMID:  12791149     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Bacterial RecA protein is required for repair of two-strand DNA lesions that disable whole chromosomes. recA mutants are viable, suggesting a considerable cellular capacity to avoid these chromosome-disabling lesions. recA-dependent mutants reveal chromosomal lesion avoidance pathways. Here we characterize one such mutant, rdgB/yggV, deficient in a putative inosine/xanthosine triphosphatase, conserved throughout kingdoms of life. The rdgB recA lethality is suppressed by inactivation of endonuclease V (gpnfi) specific for DNA-hypoxanthines/xanthines, suggesting that RdgB either intercepts improper DNA precursors dITP/dXTP or works downstream of EndoV in excision repair of incorporated hypoxathines/xanthines. We find that DNA isolated from rdgB mutants contains EndoV-recognizable modifications, whereas DNA from nfi mutants does not, substantiating the dITP/dXTP interception by RdgB. rdgB recBC cells are inviable, whereas rdgB recF cells are healthy, suggesting that chromosomes in rdgB mutants suffer double-strand breaks. Chromosomal fragmentation is indeed observed in rdgB recBC mutants and is suppressed in rdgB recBC nfi mutants. Thus, one way to avoid chromosomal lesions is to prevent hypoxanthine/xanthine incorporation into DNA via interception of dITP/dXTP.
Authors:
Jill S Bradshaw; Andrei Kuzminov
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Molecular microbiology     Volume:  48     ISSN:  0950-382X     ISO Abbreviation:  Mol. Microbiol.     Publication Date:  2003 Jun 
Date Detail:
Created Date:  2003-06-06     Completed Date:  2003-09-16     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8712028     Medline TA:  Mol Microbiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1711-25     Citation Subset:  IM    
Affiliation:
Department of Microbiology, University of Illinois at Urbana-Champaign, B103 C&LSL, 601 South Goodwin Ave., 61801-3709, USA.
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MeSH Terms
Descriptor/Qualifier:
Chromosomes, Bacterial / genetics*
DNA Damage*
DNA Repair*
Deoxyribonuclease (Pyrimidine Dimer)
Endodeoxyribonucleases / genetics,  metabolism
Escherichia coli / genetics*,  growth & development,  metabolism
Escherichia coli Proteins / genetics,  metabolism*
Exodeoxyribonuclease V
Exodeoxyribonucleases / genetics,  metabolism
Mutagenesis, Insertional
Mutation
Plasmids / genetics
Pyrophosphatases / genetics,  metabolism*
Chemical
Reg. No./Substance:
0/Escherichia coli Proteins; EC 3.1.-/Endodeoxyribonucleases; EC 3.1.-/Exodeoxyribonucleases; EC 3.1.11.5/Exodeoxyribonuclease V; EC 3.1.11.5/exodeoxyribonuclease V, E coli; EC 3.1.25.1/Deoxyribonuclease (Pyrimidine Dimer); EC 3.6.1.-/Pyrophosphatases; EC 3.6.1.-/RdgB protein, E coli

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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