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Mice carrying null mutations of the genes encoding insulin-like growth factor I (Igf-1) and type 1 IGF receptor (Igf1r).

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.

Pubmed ID: 8402901


  • Liu JP
  • Baker J
  • Perkins AS
  • Robertson EJ
  • Efstratiadis A



Publication Data

October 8, 1993

Associated Grants


Mesh Terms

  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • DNA Primers
  • Dwarfism
  • Embryo, Mammalian
  • Homozygote
  • Insulin-Like Growth Factor I
  • Mice
  • Molecular Sequence Data
  • Mutagenesis, Site-Directed
  • Phenotype
  • Point Mutation
  • Protein Conformation
  • Receptor, IGF Type 1
  • Restriction Mapping
  • Signal Transduction
  • Stem Cells