Project description:Analysis of gene expression in WT and ATRX KO Cast x 129 Mouse ES cells Paired end RNA-seq analysis of PolyA selected RNA and PolyA depeleted RNA from in both wildtype nd ATRX knocked out Castx129 Mouse ES Cells
Project description:Regions of H3.3 binding in WT and ATRX KO mouse ES cells were identified by ChIP seq Chip-seq experiements were performed in WT and ATRX KO E14 mouse ES cells
Project description:Homozygous disruption of Bteb2/Klf5, a homolog of Drosophila gap gene Krüppel, led to increased expression of various differentiation marker genes, such as Fgf5, Cdx2, and Brachyury in mouse ES cells without compromising their ability to differentiate into all three germ layers. Upon removal of LIF, Klf5-deficient ES cells showed faster differentiation kinetics than wild-type ES cells. In contrast, overexpression of Klf5 in ES cells suppressed the transcription of differentiation marker genes, and maintained pluripotency in the absence of LIF. In order to search downstream genes of Klf5, we surveyed genes implicated in ES cell proliferation by microarray analysis Keywords: cell type comparison
Project description:A majority of genetically modified mice carry passenger mutations, originating from the 129-derived embryonic stem (ES) cells, near the targeted gene. Unintended retention of these mutations can introduce confounding phenotypes and affect conclusions. We show that Ackr1-/-129ES mice retained approximately 6 Mb of 129 ES cells-derived genomic material in chromosome 1 near Ackr1 in bone marrow derived monocytes (Mono), nucleated erythroblasts (NECs), and polymorphonucleated neutrophils (PMN), notably affecting the expression of PYHIN genes.
Project description:We performed the whole genome bisulfite sequencing to detect the DNA methylation between the wild type ES cells and Smchd1 mutant ES cells