Project description:Trophoblast lineages, as the precursor of placenta, are essential for post-implantation embryo survival. However, the regulatory networks for trophoblast development remains incompletely understood. Here, we identified CITED1 as a regulator to induce trophoblast-like differentiation from mESCs. Overexpression of CITED1 in ESCs prompted differentiation towards trophoblast accompanying with elevated expression of trophoblast marker genes. To evaluate the ability of CITED1 to induce trophoblast differentiation at a genome-wide scale, we compared the global transcriptional profiles between CITED1 overexpressing cells and control ESCs by Affymetrix microarray analysis at day 1 and day 2 after transfection. We used microarrays to identify genes affected by CITED1 overexpression in mouse ESCs.
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility.
Project description:The role of mitochondria dynamics and its molecular regulators remains largely unknown during naïve-to-primed pluripotent cell interconversion. Here we report that mitochondrial MTCH2 is a regulator of mitochondrial fusion, essential for the naïve-to-primed interconversion of murine embryonic stem cells (ESCs). During this interconversion, wild-type ESCs elongate their mitochondria and slightly alter their glutamine utilization. In contrast, MTCH2-/- ESCs fail to elongate their mitochondria and to alter their metabolism, maintaining high levels of histone acetylation and expression of naïve pluripotency markers. Importantly, enforced mitochondria elongation by the pro-fusion protein Mitofusin (MFN) 2 or by a dominant negative form of the pro-fission protein dynamin-related protein (DRP) 1 is sufficient to drive the exit from naïve pluripotency of both MTCH2-/- and wild-type ESCs. Taken together, our data indicate that mitochondria elongation, governed by MTCH2, plays a critical role and constitutes an early driving force in the naïve-to-primed pluripotency interconversion of murine ESCs.
