Fgfr2III -/- mice were generated from heterozygous breedings. Embryos were harvested between embryonic day (E) 11.0 to E 13.5 and genotyped by polymerase chain reaction (PCR). Duodenums were dissected out, fixed and photographed. Whole mount and section in situs were performed for Raldh2.
Fgfr2IIIb-/- embryos demonstrate subtle changes in the duodenal morphology by E11.5 with complete involution of the atretic precursor by E聽13.5. Raldh2 appears to be down-regulated as early as E 11.5 in the atretic precursor a full 2 days before this segment disappears.
In Fgfr2IIIb-/- mouse embryos, a reduction of Raldh2 expression is observed within the region that is forming the atresia. This is the first demonstration of such an event in this model. As in humans, these results implicate disruptions between Fgfr2IIIb receptor function and RA signaling in the formation of this defect and indicate that Fgfr2IIIb-/- mouse embryos are a valid model for the study of the atretic spectrum of defects in human duodenal development.