Project description:We have analysed and compared mRNA expression between wt embryos and embryos deficient for Arid3b in E9.5 hearts, with the aim of identifying differentially expressed genes that could give us a clue to the functions of Arid3b during development.
Project description:We have analysed and compared mRNA expression between wt embryos and embryos deficient for Arid3b in E9.5 hearts, with the aim of identifying differentially expressed genes that could give us a clue to the functions of Arid3b during development. Hearts were dissected from E9.5 embryos (including the heart tube and the pharyngeal mesoderm and endoderm located beneath). Four wild-type and four mutant embryos were collected and pooled for each of the microarray triplicates.
Project description:We have analysed and compared mRNA expression between wt embryos and embryos deficient for Arid3b in E9.5 trunks, with the aim of identifying differentially expressed genes that could give us a clue to the functions of Arid3b during development.
Project description:We have analysed and compared mRNA expression between wt embryos and embryos deficient for Arid3b in E9.5 heads, with the aim of identifying differentially expressed genes that could give us a clue to the functions of Arid3b during development.
Project description:We have analysed and compared mRNA expression between wt embryos and embryos deficient for Arid3b in E9.5 heads, with the aim of identifying differentially expressed genes that could give us a clue to the functions of Arid3b during development. Heads were dissected from E9.5 embryos (including head and first branchial arch). Four wild-type and four mutant embryos were collected and pooled for each of the microarray triplicates.
Project description:We have analysed and compared mRNA expression between wt embryos and embryos deficient for Arid3b in E9.5 trunks, with the aim of identifying differentially expressed genes that could give us a clue to the functions of Arid3b during development. Trunks were dissected from E9.5 embryos (including the body from the otic vesicle to somite 15 and forelimbs). Four wild-type and four mutant embryos were collected and pooled for each of the microarray triplicates.
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.