RalGAPα1is dispensable for embryonic cortical morphogenesisin mice

Abstract Background: Cortical morphogenesis is a complex process and involves a large number of genes. RalGAPα1 gene (also called Tulip1 ), mapped to chromosome 14q13.2, is a candidate gene for the 14q13 deletion syndrome associated with delayed brain development. However, it remains unknown whether RalGAPα1 directly regulates cortical development. Methods: To address the above question, we generated neural progenitor cells (NPCs) specific RalGAPα1 conditional knockout (cKO) mice through crossing RalGAPα1 f/f to Nestin-Cre transgenic (Tg) mice in which the Cre recombinase is expressed in neural progenitor cells and derived neurons in the central nervous system (CNS) since very early stage of development. Morphological, biochemistry and immunohistochemistry (IHC) methods were used to evaluate brain development. Results: We found that the brain size, shape and cortical laminations were comparable between control and RalGAPα1 cKO mice. Moreover, the populations and proliferations of NPCs in the ventricular and subventricular zones were not different between control and RalGAPα1 cKO cortices. Conclusions: Inactivation of RalGAPα1 in the central nervous system in murine model does not significantly affect the embryonic cortical development. Keywords: RalGAPα1 ; cortical development; neural progenitor cells; neurodevelopmental disease