Project description:Purpose: to identify genes directly bound by HIF1a in cardiomycoytes Methods: crosslinked chromatin isolated from E12.5 mouse hearts was precipitated using an anti-HIF1a antibody and processed for sequencing. A list of genes containing a HIF1a peak (Minimum score 3.5) was compared with RNA-seq results to identify genes that are bound by HIF1a and expressed in E12.5 hearts Results: this analysis identified 1016 genes expressed and bound by HIF1a in embryonic hearts
Project description:Purpose: to identify genes aberrantly expressed upon myocardial ablation of Hif1a Methods: a floxed Hif1a allele was deleted in mouse embryonic hearts using a NXK2.5Cre line. Total RNA was extracted from E12.5 hearts (n=3 for controls and mutants) usinz Trizol and processed for RNA-seq. Reads were mapped to Mm10 reference genome using TopHat2 and Bowtie2. Transcript expression values were determined after transcript normalization with AltAnalyze Results: this analysis revealed a total of 1451 genes significantely (|Fold| > 20% and P<0.05) modulated in Hif1a cKO hearts 6 total RNAseq runs with 3 experimental samples and 3 controls samples
Project description:Purpose: to identify genes aberrantly expressed upon myocardial ablation of Hif1a Methods: a floxed Hif1a allele was deleted in mouse embryonic hearts using a NXK2.5Cre line. Total RNA was extracted from E12.5 hearts (n=3 for controls and mutants) usinz Trizol and processed for RNA-seq. Reads were mapped to Mm10 reference genome using TopHat2 and Bowtie2. Transcript expression values were determined after transcript normalization with AltAnalyze Results: this analysis revealed a total of 1451 genes significantely (|Fold| > 20% and P<0.05) modulated in Hif1a cKO hearts
Project description:Transcriptional profiling of the atrioventricular canal from e10.5 mouse hearts comparing wild-type control with Tbx3 GH/N hypomorphic mutant microdissected tissue. The goal was to identify direct and indirect targets of the transcription factor Tbx3, because Tbx3 is expressed in the AVC and hypomorphs develop embryonic AV conduction block at e12.5.
Project description:Transcriptional profiling of the atrioventricular canal from e10.5 mouse hearts comparing wild-type control with Tbx3 GH/N hypomorphic mutant microdissected tissue. The goal was to identify direct and indirect targets of the transcription factor Tbx3, because Tbx3 is expressed in the AVC and hypomorphs develop embryonic AV conduction block at e12.5. Two-condition experiment, wild-type control and Tbx3 mutant AVC tissue. Tissue from 5 hearts was pooled to make each sample. Biological replicates: 4.
Project description:In order to identify the targets of GATA4-FOG2 action in mammalian heart development we performed Affymetrix microarray comparisons of gene expression in normal and mutant at embryonic (E) day E12.5 hearts. We compared RNA samples from both Fog2-null and Gata4ki/ki mutant E12.5 hearts to the wild-type control E12.5 hearts. We reasoned that as the phenotypes of the Fog2 knockout and Gata4ki/ki mutation (a V217G mutation that specifically cripples the interaction between GATA4 and FOG proteins) are similar, we should expect to identify a similar set of differentially expressed genes in both experiments. As an additional control, we expected to find the Fog2 gene expression absent in the mutant (null) Fog2 cardiac sample, but not Gata4ki/ki sample.
Project description:In order to identify the targets of GATA4-FOG2 action in mammalian heart development we performed Affymetrix microarray comparisons of gene expression in normal and mutant at embryonic (E) day E12.5 hearts. We compared RNA samples from both Fog2-null and Gata4ki/ki mutant E12.5 hearts to the wild-type control E12.5 hearts. We reasoned that as the phenotypes of the Fog2 knockout and Gata4ki/ki mutation (a V217G mutation that specifically cripples the interaction between GATA4 and FOG proteins) are similar, we should expect to identify a similar set of differentially expressed genes in both experiments. As an additional control, we expected to find the Fog2 gene expression absent in the mutant (null) Fog2 cardiac sample, but not Gata4ki/ki sample. We have analyzed 6 RNA samples total (3 from control hearts, 2 from FOG2 null hearts and 1 from GATA4ki hearts)