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: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:The WHV/c-myc transgenic mouse is an animal model of hepatocarcinogenesis that can exquisitely mimic the cancer staging in human Hepatocellular carcinoma (HCC), in which the c-myc oncogene is activated by adjacent woodchuck hepatitis virus (WHV) DNA sequences. Compared to other models of c-myc transgenic mice, WHV/c-myc mice stably develop HCC with a relatively short latent period of 8 to 12 months, with a high (near 100%) tumor incidence. The aim of this study was to discover new HCC biomarkers and analyze expression patterns of selected candidate biomarkers prior to liver tumor onset by employing WHV/c-myc transgenic mice. Using Affymetrix Mouse Genome 430 2.0 Expression Arrays, we studied hepatic gene expression profiles of WHV/c-myc transgenic mice at 5 months and 11 months, age-matched wild-type C57/BL6 mice were used as controls. At 5 months, the livers of transgenic mice exhibited mild to moderate hepatocyte dysplasia, this time point represents the preneoplastic stage. At 11 months, the tumors were visualized in WHV/c-myc transgenic mice and consisted mainly of well-differentiated, trabecular-type HCCs, and this time point was considered as neoplastic stage.
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility.