Abstract：
: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.
journal_name
Celljournal_title
Cellauthors
DeChiara TM,Robertson EJ,Efstratiadis Adoi
10.1016/0092-8674(91)90513-xsubject
Has Abstractpub_date
1991-02-22 00:00:00pages
849-59issue
4eissn
0092-8674issn
1097-4172pii
0092-8674(91)90513-Xjournal_volume
64pub_type
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