Project description:Gene expression of mandibular precursor from embryonic day 13.5 trisomic and euploid embryos from the Ts65Dn Down syndrome mouse model. Results provide insight into importance of non-trisomic genes in organogenesis. Total RNA isolated from mandibular precursor of 13 trisomic and 11 euploid E13.5 embryos.
Project description:Gene expression of mandibular precursor from embryonic day 13.5 trisomic and euploid embryos from the Ts65Dn Down syndrome mouse model. Results provide insight into importance of non-trisomic genes in organogenesis.
Project description:The goal of the study was to analize expression of cell cycle related genes during postnatal development of Ts65Dn (Down syndrome mouse model) and control mice cerebellum. Keywords: Gene expression study in mouse model of disease RNA from 3 controls and 3 Ts65Dn postnatal day 2 cerebellum were analized on separate arrays.
Project description:Affymetrix Mouse Gene 1.0 ST hydridization using wt extracts from adult mice hearts as controls and Ts65Dn, Ms5Yah and Ts65Dn/Ms5Yah samples. <br><br>N = 5 mices per group of genotype.<br><br>Goal : assess the gene dosage effect on partial trisomic/monosomic mice modelling human Down syndrome.
Project description:We performed single nucleus RNA-seq and single nucleus ATAC-seq on the cortex of Ts65Dn mouse model of Down Syndrome and euploid controls (wild types).
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.
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. Hearts were taken from wide type and Myc-null Mouse embryos at E13.5 under the dissecting scope. Cardiac myocyte RNA was isolated using TRIZOL®Reagent Total RNA (100 ng) was hybridized to the Sentrix® MouseRef-8 Expression BeadChip that contains probes for ~24,000 transcripts. GeneChips were scanned using the Hewlett-Packard GeneArray Scanner G2500A. The data were analyzed with Illumina Inc. BeadStudio version 1.5.0.34 and normalized by rank invariant method.
Project description:Life Span Analysis of Brain Development, Gene Expression and Behavioral Phenotypes in the Ts1Cje, Ts65Dn and Dp16 Mouse Models of Down Syndrome
Project description:The goal of the study was to analize expression of cell cycle related genes during postnatal development of Ts65Dn (Down syndrome mouse model) and control mice cerebellum. Keywords: Gene expression study in mouse model of disease
