Strain-dependent epithelial defects in mice lacking the EGF receptor

摘要: Mice and cells lacking the epidermal growth factor receptor (EGFR) were generated to examine its physiological role in vivo. Mutant fetuses are retarded die at mid-gestation a 129/Sv genetic background, whereas x C57BL/6 cross some survive until birth even postnatal day 20 MF1 background. Death utero probably results from defect spongiotrophoblast layer of placenta. Newborn mutant mice have open eyes, rudimentary whiskers, immature lungs, defects epidermis, correlating with expression pattern EGFR as monitored by beta-galactosidase activity. These cell-autonomous because chimeric EGFR-/- embryonic stem contribute small amounts organs. indicate that regulates epithelial proliferation differentiation background influences resulting phenotype.