Project description:We performed a global mRNA expression profiling via RNA-seq. Genes differentially expressed in Mitf knock-in MEFs compared to vehicle-treated knock-in MEFs were clustered and compared to expression in untreated wild-type MEFs and primary mouse melanocytes. This clustering demonstrates a gradual transition in the expression profile of Dox-treated Mitf knock-in MEFs toward the melanocyte expression profile
Project description:To generate association of DNA methylation level and gene expression profile, we applied RNA-sequencing on mouse embryonic fibroblasts (MEFs) after the modulation of cell cycle and Dnmt1 expression level. To characterize how these factors affect somatic reprogramming, samples of MEFs induced by Yamanaka factors (Sox2, Klf4, Oct4, cMyc) was also included. The cell cycle was accelerated by shRNA targeted to p53, and the expression of Dnmt1 was manipulated by either over expression or knock down.
Project description:Using ATAC seq analysis, we showed that the MEFs with a knockout of Lmna gene (i.e., missing the lamin A/C nuclear scaffolding protein) (Lmna-/- MEFs) display a striking change in chromatin accessibility landscape (peak signals that are both up and down), both within and outside lamina-associated domains (LADs); moreover, there was a clear overrepresentation of peaks with a gain in chromatin accessibility (within and outside LADs) in the Lmna-/- MEFs, and within LADs compared to outside LADs.
Project description:MEFs treated by compounds for 25 days can be induced into astrocytes. In induced astrocytes, specific astrocytes-related sets of genes are up-regulated, but fibroblasts-related genes are down-regulated.
Project description:MEFs treated by compounds for 25 days can be induced into astrocytes. In induced astrocytes, specific astrocytes-related sets of genes are up-regulated, but fibroblasts-related genes are down-regulated. The induced cells sorted for GFP-positive cells by flow cytometry and primary astrocytes and MEFs were parepared for RNA extraction and hybridization on Affymetrix microarrays. We sought to compare the induced astrocytes with primary astrocytes and MEFs.
Project description:To compare the the genomic profile of MEFs, immature Sertoli, mature Sertoli cells, and MEFs (NWD) after infection of Nr5a1, Wt1 and Dmrt1 after 1 month of dox exposure.
Project description:In order to investigate what signalling pathways are turned on by tenascin-C, we generated Mouse Embryonic Fibroblasts (MEFs) deficient for tenascin-C and compared their gene expression profile to MEFs proficient for tenascin-C. TNC-KO MEFs as well as WT MEFs in which tenascin-C was knocked-down (following stable transfection of a short hairpin RNA) were compared to WT MEFs (expressing strong endogenous levels of tenascin-C).
Project description:Purpose: To gain insights into the activity of Cyclin D1 in tumor maintenance, we developed a specific RNAi strategy to knock down its expression and analyze the outcome on gene expression profile of RAS/DNP53-driven cancer cells (transformed MEFs). Cells were treated by RNAi or with Leptomycin B over night. Method: RAS/DNP53-transformed MEFs mRNA profiles were generated by RNA-Sequencing. Results: Cyclin D1 knock down in RAS-G12V-driven cancer cells leads to expression change of genes involved in developmental processes, but no change in FAS or FASL levels.
Project description:SMRT (silencing mediator of retinoid and thyroid hormone receptors) is recruited by numerous transcription factors to mediate lineage and signal dependent transcriptional repression. We generated a knock-in mutation in the receptor interaction domain (RID) of SMRT (SMRTmRID) that solely disrupts its interaction with nuclear hormone receptors. SMRTmRID-derived 3T3-MEFs display a dramatically increased adipogenic capacity and accelerated differentiation rate. We measured global gene expression in wild-type versus SMRTmRID-derived 3T3-MEFs in the undifferentiated state to examine which pathways were altered. Our results demonstrate that SMRT-RID dependent repression is a key determinant of the adipogenic set point. Keywords: SMRTmRID expression compared to wild-type
