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Publication : Parental imprinting of the mouse insulin-like growth factor II gene.

First Author  DeChiara TM Year  1991
Journal  Cell Volume  64
Issue  4 Pages  849-59
PubMed ID  1997210 Mgi Jnum  J:11007
Mgi Id  MGI:59449 Doi  10.1016/0092-8674(91)90513-x
Citation  DeChiara TM, et al. (1991) Parental imprinting of the mouse insulin-like growth factor II gene. Cell 64(4):849-59
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.
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