Liu JP, Baker J, Perkins AS, Robertson EJ, Efstratiadis AMice carrying null mutations of the genes encoding insulin-like growth factor-I (IGF-1) and type-1 IGF receptor (IGF1r). Cell 75: 59-72

ArticleinCell 75(1):59-72 · November 1993with3,285 Reads
DOI: 10.1016/S0092-8674(05)80084-4 · Source: PubMed
Abstract
Newborn mice homozygous for a targeted disruption of insulin-like growth factor gene (Igf-1) exhibit a growth deficiency similar in severity to that previously observed in viable Igf-2 null mutants (60% of normal birthweight). Depending on genetic background, some of the Igf-1(-/-) dwarfs die shortly after birth, while others survive and reach adulthood. In contrast, null mutants for the Igf1r gene die invariably at birth of respiratory failure and exhibit a more severe growth deficiency (45% normal size). In addition to generalized organ hypoplasia in Igf1r(-/-) embryos, including the muscles, and developmental delays in ossification, deviations from normalcy were observed in the central nervous system and epidermis. Igf-1(-/-)/Igf1r(-/-) double mutants did not differ in phenotype from Igf1r(-/-) single mutants, while in Igf-2(-)/Igf1r(-/-) and Igf-1(-/-)/Igf-2(-) double mutants, which are phenotypically identical, the dwarfism was further exacerbated (30% normal size). The roles of the IGFs in mouse embryonic development, as revealed from the phenotypic differences between these mutants, are discussed.

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Article
October 1993 · Cell
    Newborn mice homozygous for a targeted disruption of insulin-like growth factor gene (Igf-1) exhibit a growth deficiency similar in severity to that previously observed in viable Igf-2 null mutants (60% of normal birthweight). Depending on genetic background, some of the Igf-1(-/-) dwarfs die shortly after birth, while others survive and reach adulthood. In contrast, null mutants for the Igf1r... [Show full abstract]
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    November 1993 · Cell
      A developmental analysis of growth kinetics in mouse embryos carrying null mutations of the genes encoding insulin-like growth factor I (IGF-I), IGF-II, and the type 1 IGF receptor (IGF1R), alone or in combination, defined the onset of mutational effects leading to growth deficiency and indicated that between embryonic days 11.0 and 12.5, IGF1R serves only the in vivo mitogenic signaling of... [Show full abstract]
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        Mutations introduced into the genes encoding the insulin-like growth factors (IGF) and their receptors indicate that these molecules play critical roles in regulating embryonic growth from mid-gestation onwards. Studies of compound mutations show that IGFI, interacting with the IGF type-1 receptor (IGF1R), has important growth promoting activities in the embryo. Similarly while IGFII signals... [Show full abstract]
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