Linked Life Data

12531022

Source:http://linkedlifedata.com/resource/pubmed/id/12531022

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2003-1-17
pubmed:abstractText
Deficiency in DNA mismatch repair (MMR) confers instability of simple repeated sequences and increases susceptibility to cancer. Some of the MMR genes are also implicated in other repair and cellular processes related to DNA damage response. Supposedly, lack of their function can lead to a global genomic instability, besides microsatellite instability (MSI). To study the spontaneous and induced genomic instability in germ cells, related to the Msh2 status, DNA alterations in the progeny of individual crosses of Drosophila deficient in one or two copies of the Msh2 gene, were analysed by the arbitrarily primed polymerase chain reaction (AP-PCR). The results indicate that the progeny of homozygous parents for the normal Msh2 allele (+/+) presents a significantly lower frequency of genomic alterations than those from heterozygous (+/-) or mutant homozygous (-/-) parents. In addition, the DNA damage transmitted to the progeny, after the adult parental males were exposed to bleomycin, indicates that whereas the induction of mutations related to MSI depends on the lack of the Msh2 function, the induction of other mutational events may require at least one functional Msh2 allele. Thus, the results obtained with heterozygous individuals may have special relevance for cancer development since they show that a disrupted Msh2 allele is enough to generate genomic instability in germ cells, increasing the genomic damage in the progeny of heterozygous individuals. This effect is enhanced by mutagenic stress, such as occurs after bleomycin exposure.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1568-7864
pubmed:author
pubmed:issnType
Print
pubmed:day
3
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
941-54
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12531022-Animals, pubmed-meshheading:12531022-Antimetabolites, Antineoplastic, pubmed-meshheading:12531022-Base Pair Mismatch, pubmed-meshheading:12531022-Bleomycin, pubmed-meshheading:12531022-Crosses, Genetic, pubmed-meshheading:12531022-DNA, pubmed-meshheading:12531022-DNA Damage, pubmed-meshheading:12531022-DNA Fingerprinting, pubmed-meshheading:12531022-DNA Primers, pubmed-meshheading:12531022-DNA Repair, pubmed-meshheading:12531022-Drosophila Proteins, pubmed-meshheading:12531022-Drosophila melanogaster, pubmed-meshheading:12531022-Electrophoretic Mobility Shift Assay, pubmed-meshheading:12531022-Genome, pubmed-meshheading:12531022-Male, pubmed-meshheading:12531022-Microsatellite Repeats, pubmed-meshheading:12531022-Mutation, pubmed-meshheading:12531022-Polymerase Chain Reaction, pubmed-meshheading:12531022-Recombinant Proteins, pubmed-meshheading:12531022-Repressor Proteins, pubmed-meshheading:12531022-Trans-Activators
pubmed:year
2002
pubmed:articleTitle
Spontaneous and bleomycin-induced genomic alterations in the progeny of Drosophila treated males depends on the Msh2 status. DNA fingerprinting analysis.
pubmed:affiliation
Grup de Mutagènesi, Unitat de Genètica, Departament de Genètica i de Microbiologia, Edifici Cn, Universitat Autònoma de Barcelona, 08193 Bellaterra, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't