Document Detail


Mutations arising during repair of chromosome breaks.
MedLine Citation:
PMID:  23146099     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Mutations stimulate evolutionary change and lead to birth defects and cancer in humans as well as to antibiotic resistance in bacteria. According to the classic view, most mutations arise in dividing cells and result from uncorrected errors of S-phase DNA replication, which is highly accurate because of the involvement of selective DNA polymerases and efficient error-correcting mechanisms. In contrast, studies in bacteria and yeast reveal that DNA synthesis associated with repair of double-strand chromosomal breaks (DSBs) by homologous recombination is highly inaccurate, thus making DSBs and their repair an important source of mutations. Different error-prone mechanisms appear to operate in different repair scenarios. In the filling in of single-stranded DNA regions, error-prone translesion DNA polymerases appear to produce most errors. In contrast, in gene conversion gap repair and in break-induced replication, errors are independent of translesion polymerases, and many mutations have the signatures of template switching during DNA repair synthesis. DNA repair also appears to create complex copy-number variants. Overall, homologous recombination, which is traditionally considered a safe pathway of DSB repair, is an important source of mutagenesis that may contribute to human disease and evolution.
Authors:
Anna Malkova; James E Haber
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Annual review of genetics     Volume:  46     ISSN:  1545-2948     ISO Abbreviation:  Annu. Rev. Genet.     Publication Date:  2012  
Date Detail:
Created Date:  2012-11-13     Completed Date:  2013-04-22     Revised Date:  2013-05-09    
Medline Journal Info:
Nlm Unique ID:  0117605     Medline TA:  Annu Rev Genet     Country:  United States    
Other Details:
Languages:  eng     Pagination:  455-73     Citation Subset:  IM    
Affiliation:
Department of Biology, School of Science, IUPUI, Indianapolis, Indiana 46202-5132, USA. amalkova@iupui.edu
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Biological
Chromosome Breakage*
Chromosomes, Bacterial / genetics*
Chromosomes, Fungal / genetics
Crossing Over, Genetic
DNA Breaks, Double-Stranded*
DNA Copy Number Variations
DNA Repair*
DNA Replication*
DNA, Bacterial / genetics
DNA, Fungal / genetics
Escherichia coli / genetics
Mutagenesis
Mutation*
Saccharomycetales / genetics
Grant Support
ID/Acronym/Agency:
GM084242/GM/NIGMS NIH HHS; GM20056/GM/NIGMS NIH HHS; GM61766/GM/NIGMS NIH HHS; GM76020/GM/NIGMS NIH HHS; R01 GM076020/GM/NIGMS NIH HHS; R37 GM020056/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/DNA, Bacterial; 0/DNA, Fungal

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


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