Project description:Global loss of SLMAP3 resulted in developmental defects, therefore we wanted to analyze developmental gene expression in SLMAP3-knockout embryos when compared to wildtype embryos.
Project description:The development of vertebrate extremities is a complex process which requires a highly coordinated network of different transcriptional activities. The homeodomain transcription factor Shox2 is a key player in limb formation controlling neural, muscular and skeletal development. Here, we compared gene expression profiles of wildtype and Shox2 knockout limbs using microarray experiments to identify Shox2 target genes. Forelimbs of E11.5 mouse embryos were dissected and genotyped for RNA extraction. RNA from 3-4 embryos of 2 different pregnancies was used for hybridisation to 2 arrays per genotype (wildtype and Shox2 knockout) and compared.
Project description:The Hippo signaling pathway is known to regulate cell differentiation, proliferation and apoptosis. The WWC proteins, WWC1 and WWC2, positively regulate the Hippo pathway by the activation of the LATS kinases and the subsequent cytoplasmic translocation of YAP. The in vivo role of WWC2 has not been studied, yet. We could show, that the ubiquitous knockout of WWC2 in mice leads to placental defects, growth retardation, a disturbed angiogenesis and vascularization resulting in embryonic lethality at around E11.5. To further understand the function of WWC2 in the embryonic development, a transcriptome analysis by next generation sequencing was performed.
Project description:Dnmt3b is a DNA methyltransferase, an enzyme which methylates genomic DNA, contributes to genomic stability and transcriptional regulation. Inactivation of Dnmt3b in mice results in embryonic lethality at E13.5. It is however unclear which activities are responsible for this phenomenon. Here, we analyzed methylation and gene expression in Dnmt3b+/+ (WT), Dnmt3b-/- (3bKO) and Dnmt3bCI/CI (3bKI) embryos at E11.5.
Project description:Targeted deletion of skNAC in mice resulted in early embryonic lethality with cardiac defects. In order to investigate the molecular mechanism of the cardiac defect, we designed the microarray comparing gene expression of the mutant E11.5 heart to wild type E11.5 heart. Keywords: genetic modification in mouse