Project description:Flvcr1 is a heme transporter involved in multiple processes. Here we invetigated the role of this transporter in brain development in mice. Deletion of Flvcr1 in nerual progenitors leads to metabolic collapse of neural progenitors and cortical disruption. Using transcriptional profiling, we show that brains of these embryos expressed reduced levels of electron transport chain components and increased levels of heme metabolic genes. These results implicate Flvcr1 in brain development through control of the metabolic state in neural progenitors.
Project description:The high-density lipoprotein receptor SR-B1 mediates cellular uptake of several lipid species, including cholesterol and vitamin E. During early development, SR-B1 is located in the maternal-fetal interface, where it facilitates vitamin E transport towards the embryo. Consequently, embryos lacking SR-B1 are vitamin E-deficient, and around half of them fail to close the neural tube and show neural tube defects (NTD). Here, we studied the transcriptomic profile of mouse embryos lacking SR-B1 to identify the molecular determinants of this phenotypic difference. We used RNA-Seq to analyze the expression of mRNA globally in E9.5 wild-type embryos and embryos lacking SR-B1 with or without NTD, in order to compare expression profiles in those groups and to identify putative genes driving phenotypic differences.
Project description:Tgfbr2 controls signal transduction after binding activated Tgfb1. Inactivation of this receptor in endothelium results in vascular dysplasia and severe hemorrhage. Here, we define the transcriptional profile of endothelial cells lacking Tgfbr2.