Expression Pattern of Dab1, Reelin, PGP9.5 and Sox2 in the Stomach of () Mice.

: The Reelin-Dab1 signaling pathway, known for its crucial role in neurodevelopment, particularly in neuronal migration and the formation of cortical layers, has been a subject of extensive research. However, its involvement in gastrointestinal organogenesis is a relatively unexplored area. Our study investigates the expression patterns of Dab1, Reelin, PGP9.5, and Sox2 during stomach development in () mice and aims to shed light on how inactivation affects epithelial-mesenchymal signaling dynamics, thereby contributing to a deeper understanding of this pathway's non-neural functions. : Embryonic stomach tissues from and wild-type mice, collected at developmental stages E13.5 and E15.5, were examined by immunofluorescenceto evaluate the difference in expression of Dab1, Reelin, PGP9.5, and Sox2. Semi-quantitative scoring and quantitative image analysis were used to assess protein localization and intensity within epithelial and mesenchymal compartments. : Dab1 expression was significantly increased in both the epithelium and mesenchyme of mice at E13.5 and E15.5. Reelin expression in the epithelium showed a visible but statistically non-significant decrease in at E15.5, while mesenchymal expression remained low and significantly lower than controls. PGP9.5 expression was significantly reduced in epithelium at E13.5, then strongly upregulated at E15.5. Mesenchymal PGP9.5 remained consistently high. Sox2 showed no statistically significant changes but increased semi-quantitatively in epithelium and mesenchyme at E15.5. These findings highlight compartment-specific disruptions and potential compensatory mechanisms following inactivation. : Our findings indicate that deficiency leads to distinct molecular changes in epithelial and mesenchymal compartments of the developing stomach. The Reelin-Dab1 axis appears critical for epithelial-mesenchymal coordination, while PGP9.5 and Sox2 upregulation in mice may represent potential compensatory responses that could support epithelial integrity, although this remains speculative without functional validation.