Genes & Development · 1994 · 607 citations · 52 references
Life SciencesGeneticsMolecular GeneticsDevelopmental GeneticsEmbryogenesisGene ExpressionCardiovascular DevelopmentFetal DevelopmentFetal GrowthFetal PhysiologyGenomic ImprintingHeart DevelopmentCardiac Developmental PhysiologyCardiovascular Developmental EffectsEmbryologic Heart DevelopmentFetal Growth Regulation By ImprintingImprinting In EmbryogenesisImprinting In Mammalian DevelopmentInsulin-like Growth Factor GeneticsInsulin-like Growth Factors
Murine embryos that inherit a nonfunctional insulin-like growth factor-II/cation-independent mannose 6-phosphate receptor (Igf2r) gene from their fathers are viable and develop normally into adults. However, the majority of mice inheriting the same mutated allele from their mothers die around birth, as a consequence of major cardiac abnormalities. These mice do not express IGF2R in their tissues, are 25-30% larger than their normal siblings, have elevated levels of circulating IGF2 and IGF-binding proteins, and exhibit a slight kink in their tails. These results show that Igf2r is paternally imprinted and reveal that the receptor is crucial for regulating normal fetal growth, circulating levels of IGF2, and heart development.
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Cleavage of Structural Proteins during the Assembly of the Head of Bacteriophage T4
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