Targeted Disruption of Mouse EGF receptor: Effect of Genetic Background on Mutant Phenotype
David W. Threadgill(Case Western Reserve University), Andrzej A. Dlugosz(National Institutes of Health), Laura A. Hansen(National Institutes of Health), Tamar Tennenbaum(National Institutes of Health), Ulrike Lichti(National Institutes of Health), Della Yee(Case Western Reserve University), Christian LaMantia(Case Western Reserve University), Tracy Mourton(Case Western Reserve University), Karl Herrup(Case Western Reserve University), Raymond C. Harris(Vanderbilt University), John Barnard(Vanderbilt University), Stuart H. Yuspa(National Institutes of Health), Robert J. Coffey(Vanderbilt University), Terry Magnuson(Case Western Reserve University)
Cited by 1,467
Abstract
Gene targeting was used to create a null allele at the epidermal growth factor receptor locus (Egfr). The phenotype was dependent on genetic background. EGFR deficiency on a CF-1 background resulted in peri-implantation death due to degeneration of the inner cell mass. On a 129/Sv background, homozygous mutants died at mid-gestation due to placental defects; on a CD-1 background, the mutants lived for up to 3 weeks and showed abnormalities in skin, kidney, brain, liver, and gastrointestinal tract. The multiple abnormalities associated with EGFR deficiency indicate that the receptor is involved in a wide range of cellular activities.
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