Project description:Atypical protein kinase C iota (Prkci) knockout mice are embryonic lethal at gestation day 9.5 but the underlying molecular mechanisms is not known. Here , using Prkci knockout mouse model , we show that trophectoderm specific function of PKCi is essential for post-implantation mammalian development. We observed that PKCi is expressed predominantly in the trophectoderm lineage and developing placenta region in post-implantation mouse embryos. Prkci knockout or homozygous embryos show severe defect in placenta formation compared to wildtype and heterozygous embryos. Using RNA seq analysis in PKCi knockdown mouse trophoblast stem cells, we identified certain genes which are significantly upregulated upon PKCi depletion , one among them is Bone Morphogenetic protein 13 (Bmp13). Our study shows that PKCi is one of key players involved in proper development of the placenta, loss of which might be one of the reasons for early pregnancy failure.
Project description:The placenta establishes a maternal–fetal exchange interface which ensures transportation of nutrients and gases between the mother and the fetus. However, the intricate molecular processes and gene expression dynamics in trophoblast progenitors and in matured trophoblast cells are incopletely understood. Therefor, in this study we performed gene expression analyses during the course of mouse placenta development. We performed single cell RNA-sequencing analyses with mouse placenta primordium at embryonic day 7.0 and subsequently at embryonic days 8.5-embryonic day 12.5 to capture gene expression dynamics in trophoblast stem/progenitor compartment as well as in matutered trophoblast cells and other cell types in the placenta.
