International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


POSTER 94 - MOLECULAR AND GENETIC ANALYSIS OF THE EPIDERMAL GROWTH FACTOR RECEPTOR IN MURINE PLACENTAL DEVELOPMENT

Ms. Karen Strunk
University of North Carolina-Chapel Hill
Department of Genetics
11-109 Lineberger Cancer Center
Campus Box #7264
Chapel Hill NC 27599-7264
USA

Co-Authors: Hovick M, Amann V, Threadgill DW
Institutions: University of North Carolina, Department of Genetics

Homozygous epidermal growth factor receptor (Egfr) null mutants exhibit peri-implantation to post-natal lethality, depending on the genetic background. On a 129/SvEvTAC background Egfr homozygous null embryos die at embryonic day 11.5 due to placental defects. The placentae show a decreased size compared to those from control littermates, with a reduced spongiotrophoblast layer and disorganization of the labyrinthine layer. On an outbred CD-1 background homozygous null pups also exhibit a reduced spongiotrophoblast layer, but there is partial rescue of the labyrinthine layer. To address the strain dependant variability, a scan for genetic modifiers was performed using the outbred CD-1 background. No statistically significant loci were identified in a large backcross mapping panel. In order to partition the genetic variability potentially segregating within the outbred Swiss-derived CD-1 population, we tested 10 inbred Swiss-derived strains to determine the viability of Egfr null mutants. The strains tested include ALR/LtJ, ALS/LtJ, NON/LtJ, NOD/LtJ, ICR/HaRos, SJL/J, SWR/J, FVB/NJ, APN, and APS. We reasoned that different inbred strains derived from the same Swiss population as the outbred CD-1 mice would have captured different sets of modifier alleles. As predicted, a significant variation in the penetrance of Egfr null viability was observed in the various inbred strains.


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