Linked Life Data

1997210

Source:http://linkedlifedata.com/resource/pubmed/id/1997210

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1991-4-2
pubmed:abstractText
We are studying mice that carry a targeted disruption of the gene encoding insulin-like growth factor II (IGF-II). Transmission of this mutation through the male germline results in heterozygous progeny that are growth deficient. In contrast, when the disrupted gene is transmitted maternally, the heterozygous offspring are phenotypically normal. Therefore, the difference in growth phenotypes depends on the type of gamete contributing the mutated allele. Homozygous mutants are indistinguishable in appearance from growth-deficient heterozygous siblings. Nuclease protection and in situ hybridization analyses of the transcripts from the wild-type and mutated alleles indicate that only the paternal allele is expressed in embryos, while the maternal allele is silent. An exception is the choroid plexus and leptomeninges, where both alleles are transcriptionally active. These results demonstrate that IGF-II is indispensable for normal embryonic growth and that the IGF-II gene is subject to tissue-specific parental imprinting.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0092-8674
pubmed:author
pubmed:issnType
Print
pubmed:day
22
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
849-59
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Parental imprinting of the mouse insulin-like growth factor II gene.
pubmed:affiliation
Department of Genetics and Development, Columbia University, New York, New York 10032.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.