Project description:The aim of this experiment was to investigate the role of KLF1 in the fetal liver Affymetrix microarrays were performed on fetal liver cells from E13.5 wildtype and Klf1-/- mice. Three wildtype replicates and three Klf1-/- replicates, all from E13.5 fetal liver.
Project description:The aim of this experiment was to investigate the role of KLF1 in the fetal liver Affymetrix microarrays were performed on fetal liver cells from E13.5 wildtype and Klf1-/- mice.
Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Keywords: wildtype vs Myc-null
Project description:The aim of this experiment was to investigate the regulation of gene expression by KLF3 and KLF8 in fetal erythroid cells by analyzing single and double mutant mouse models. Affymetrix microarrays were performed on RNA from TER119+ fetal liver cells from E13.5 wildtype, Klf8gt/gt, Klf3-/- and Klf3-/- Klf8gt/gt mice. Four wildtype replicates, four Klf8gt/gt replicates, three Klf3-/- replicates and four Klf3-/- Klf8gt/gt replicates of E13.5 TER119+ fetal liver cell samples, litter-matched where possible.
Project description:PGCs undergo two distinct stages of demethylation before reaching a hypomethylated ground state at E13.5. Stage 1 occurs between E7.25- E9.5 in which PGCs experience a global loss of cytosine methylation. However, discreet loci escape this global loss of methylation and between E10.5-E13.5, stage 2 of demethylation takes place. In this stage these loci are targeted by Tet1 and Tet2 leading to the loss of the remaining methylation and resulting in the epigenetic ground state. Our data shows that Dnmt1 is responsible for maintaining the methylation of loci that escape stage 1 demethylation, and that it functions in a UHRF1 independent manner. Our data further demonstrates that when these loci lose methylation prior to stage 2 it results in early activation of the meiotic program, which leads to precocious differentiation of the germ line resulting in a decreased pool of PGCs in the embryo and subsequent infertility in adult mice.