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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1382
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pubmed:dateCreated |
1997-7-17
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pubmed:abstractText |
Genomically imprinted genes are those for which expression is dependent on the sex of the parent from which they are derived. Numerous theories have been proposed for the evolution of genomic imprinting: one theory is that it is an intra-individual manifestation of classical parent -offspring conflict. This theory is unique in predicting that an arms race may develop between maternally and paternally derived genes for the control of foetal growth demands. Such antagonistic coevolution may be mediated through changes in the structure of the proteins concerned. Comparable coevolution is the most likely explanation for the rapid changes seen in antigenic components of parasites and antigen recognition components of immune systems. We have examined the evolution of insulin-like growth factor Igf2, and its antagonistic receptor Igf2r) and find that in contrast to immune genes, at the sites of mutual binding they are highly conserved. In addition, we have analysed the rate of molecular evolution of seven imprinted genes including Igf2 and Igf2r), sequenced in both mouse and rat, and had that this is the same as that of nonimprinted receptors and significantly lower than that of immune genes controlling for differences in mutation rates. Contrary to the expectations of the conflict hypothesis, we hence find no evidence for antagonistic coevolution of imprinted genes mediated by changes in sequence.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-1657932,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-1706291,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-1732164,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-1848481,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-2035190,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-2283951,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-3412472,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-3916709,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-7629109,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-7689653,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-7773285,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-7797478,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-7877487,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-7896100,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-7928394,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8032205,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8083887,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8115596,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8188212,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8308912,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8462995,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8516846,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8589711,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8639158,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8676743,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8786129,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8812454,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8828237,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8831294,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8852860,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8913768,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-8977873,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9178545-9781817
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0962-8452
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
22
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pubmed:volume |
264
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
739-46
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:9178545-Amino Acid Sequence,
pubmed-meshheading:9178545-Animals,
pubmed-meshheading:9178545-Base Sequence,
pubmed-meshheading:9178545-Binding Sites,
pubmed-meshheading:9178545-Conserved Sequence,
pubmed-meshheading:9178545-Embryonic and Fetal Development,
pubmed-meshheading:9178545-Evolution, Molecular,
pubmed-meshheading:9178545-Female,
pubmed-meshheading:9178545-Genomic Imprinting,
pubmed-meshheading:9178545-Insulin-Like Growth Factor II,
pubmed-meshheading:9178545-Male,
pubmed-meshheading:9178545-Mice,
pubmed-meshheading:9178545-Models, Genetic,
pubmed-meshheading:9178545-Parasites,
pubmed-meshheading:9178545-Rats,
pubmed-meshheading:9178545-Receptor, IGF Type 2,
pubmed-meshheading:9178545-Sequence Alignment
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pubmed:year |
1997
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pubmed:articleTitle |
Molecular evolution of imprinted genes: no evidence for antagonistic coevolution.
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pubmed:affiliation |
School of Biology and Biochemistry, University of Both, Clarcton Don, UK. gatnv@mole.bio.cam.ac.uk
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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