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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
1984-1-7
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pubmed:abstractText |
A two-step model to explain the high frequency of mutation at the diploid adenine phosphoribosyltransferase (aprt) locus in CHO cells has been proposed previously (Simon et al., Mol. Cell. Biol. 2:1126-1133, 1982). This model indicates that two distinct classes of aprt heterozygotes can be isolated. Class 1 heterozygotes, the most abundant class, were defined as those which arose spontaneously and were capable of undergoing mutation to the APRT- phenotype only at a low frequency (putative point mutation). Class 2 heterozygotes arose from a mutation and gave rise at a high frequency to APRT- cells. This high-frequency event has been identified as a deletion of the wild-type allele (A. E. Simon and M. W. Taylor, Proc. Natl. Acad. Sci. U.S.A. 80:810-814, 1983). In this paper we report further analysis of class 1 heterozygotes with respect to genetic structure, gene products, and karyotype. Our study indicated that class 1 heterozygotes contain two different types of mutants. About half have only one copy of the aprt gene and an unaltered karyotype, indicating that a deletion (similar to the high-frequency second-step event observed for class 2 heterozygotes) rather than a loss of the chromosome was responsible for the generation of the aprt+/- genotype. The remainder of the previously designated class 1 heterozygotes still contained two copies of the aprt gene (within the limits of the quantitation technique used) and arose presumably by a point mutation. One of this group, D423, was characterized with respect to aprt gene products and found to produce an electrophoretic variant in addition to the wild-type protein. APRT- mutants derived from D423 retained the same number of aprt gene copies as D423 and still synthesized a protein that comigrated with wild type, unlike APRT- mutants derived from class 2 heterozygotes. D423 and the other heterozygotes with two aprt genes therefore did not fit into either class 1 or 2 and are now designated class 3. The model we present suggests that only one of the two aprt alleles present in wild-type cells can undergo the deletion.
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pubmed:grant | |
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/6646118-355893,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6646118-423774,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6646118-6253938,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6646118-6291042,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6646118-6298600,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6646118-6891022,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6646118-7101104,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6646118-7360155,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6646118-7460013
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2,6-diaminopurine,
http://linkedlifedata.com/resource/pubmed/chemical/2-Aminopurine,
http://linkedlifedata.com/resource/pubmed/chemical/8-azaadenine,
http://linkedlifedata.com/resource/pubmed/chemical/Adenine,
http://linkedlifedata.com/resource/pubmed/chemical/Adenine Phosphoribosyltransferase,
http://linkedlifedata.com/resource/pubmed/chemical/Pentosyltransferases
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0270-7306
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
3
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1703-10
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:6646118-2-Aminopurine,
pubmed-meshheading:6646118-Adenine,
pubmed-meshheading:6646118-Adenine Phosphoribosyltransferase,
pubmed-meshheading:6646118-Animals,
pubmed-meshheading:6646118-Cell Line,
pubmed-meshheading:6646118-Chromosome Deletion,
pubmed-meshheading:6646118-Cricetinae,
pubmed-meshheading:6646118-Cricetulus,
pubmed-meshheading:6646118-Drug Resistance,
pubmed-meshheading:6646118-Female,
pubmed-meshheading:6646118-Fibroblasts,
pubmed-meshheading:6646118-Heterozygote,
pubmed-meshheading:6646118-Models, Genetic,
pubmed-meshheading:6646118-Mutation,
pubmed-meshheading:6646118-Ovary,
pubmed-meshheading:6646118-Pentosyltransferases
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pubmed:year |
1983
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pubmed:articleTitle |
Mechanism of mutation at the aprt locus in Chinese hamster ovary cells: analysis of heterozygotes and hemizygotes.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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