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 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 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 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 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 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 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
