Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-6-5
pubmed:abstractText
In order to investigate the influence of loss of heterozygosity (LOH) events on mutation rate, we studied two closely related human lymphoblastoid cell lines, AHH-1 (h2E1.v2) and MCL-5, which are heterozygous at the tk locus (chromosome 17q23-25). Although they have similar mutant fractions at the hprt locus, the mutant fraction and rate at tk is four to five times higher in AHH-1. Analysis of 58 spontaneous TK- mutants from AHH-1 and MCL-5 showed that the occurrence of LOH events was more frequent (23/24) in AHH-1 than MCL-5 (16/34). A set of five microsatellite polymorphism loci was used to map the extent of LOH along chromosome 17q. In AHH-1 cells, 15/23 of the LOH events encompassed at least 35% of the sex-averaged genetic length of chromosome 17q (98 cM). Additionally, the next most extensive category of LOH accounted for 5/23 TK- mutants, and encompassed at least 17 cM. In contrast, LOH events observed in MCL-5 are very restricted in extent; only one LOH tract extended as far as 4 cM from tk. The higher mutation rate at tk in AHH-1 can, therefore, be entirely attributed to the recovery of chromosomal scale LOH in viable, normal growth TK- mutants. Furthermore, these data demonstrate that the regional potential for LOH is likely to be an important determinant of mutation rate for loci within that chromosomal segment.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0267-8357
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:geneSymbol
hprt
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
53-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:7739402-Aminacrine, pubmed-meshheading:7739402-Amino Acid Sequence, pubmed-meshheading:7739402-Base Sequence, pubmed-meshheading:7739402-Cell Line, pubmed-meshheading:7739402-Chromosomes, Human, Pair 17, pubmed-meshheading:7739402-DNA, Satellite, pubmed-meshheading:7739402-Frameshift Mutation, pubmed-meshheading:7739402-Genotype, pubmed-meshheading:7739402-Humans, pubmed-meshheading:7739402-Hypoxanthine Phosphoribosyltransferase, pubmed-meshheading:7739402-Lymphocytes, pubmed-meshheading:7739402-Molecular Sequence Data, pubmed-meshheading:7739402-Mutagenesis, pubmed-meshheading:7739402-Mutagens, pubmed-meshheading:7739402-Mutation, pubmed-meshheading:7739402-Nitrogen Mustard Compounds, pubmed-meshheading:7739402-Polymorphism, Genetic, pubmed-meshheading:7739402-Thymidine Kinase, pubmed-meshheading:7739402-Transfection
pubmed:year
1995
pubmed:articleTitle
Extensive loss of heterozygosity accounts for differential mutation rate on chromosome 17q in human lymphoblasts.
pubmed:affiliation
Environmental Toxicology Graduate Program, University of California, Riverside 92521, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't