Project description:We investigated the cardiac transcription network driven by the DNA-binding key factor Srf in combination with epigenetic marks of histone 3 acetylation (H3ac). Srf has been shown to play a key role in cardiac cell growth and muscle gene regulation. However, we still have limited understanding of the global transcription network driven by this factor in a direct or indirect manner. Moreover, we lack knowledge to which extent epigenetic marks such as histone modifications interfere with the regulation of direct targets. To gain insights into the transcriptional regulatory network two independent chromatin immunoprecipitation (ChIP) samples were profiled. DNA fragments bound to Srf or modified with acetylated histone 3 in mouse cardiomyocytes (HL1-cells) were sequenced using ultra-high throughput DNA sequencing. ChIP-seq profile of a transcription factor (Srf) and a histone modification (H3ac)
Project description:We investigated the cardiac transcription network driven by the DNA-binding key factor Srf in combination with epigenetic marks of histone 3 acetylation (H3ac). Srf has been shown to play a key role in cardiac cell growth and muscle gene regulation. However, we still have limited understanding of the global transcription network driven by this factor in a direct or indirect manner. Moreover, we lack knowledge to which extent epigenetic marks such as histone modifications interfere with the regulation of direct targets. To gain insights into the transcriptional regulatory network two independent chromatin immunoprecipitation (ChIP) samples were profiled. DNA fragments bound to Srf or modified with acetylated histone 3 in mouse cardiomyocytes (HL1-cells) were sequenced using ultra-high throughput DNA sequencing.
Project description:We report the application of chromatin immunoprecipitation sequencing to identify binding sites of the transcription factor serum response factor (SRF) in the cornea of WT and Dstn-corn1 mutant mice Examination of SRF binding sites in WT and Dstn-corn1 mutant cornea
Project description:We used an in vitro cardiomyocyte differentiation system with inducible Hey1 or Hey2 expression to study target gene regulation in cardiomyocytes (CM) generated from murine embryonic stem cells (ESC). The effects of Hey1 and Hey2 are largely redundant, but cell type specific. The number of regulated genes is comparable between ESC and CM, but the total number of binding sites is much higher, especially in ESC, targeting mainly genes involved in transcriptional regulation and developmental processes. Repression by Hey generally correlates with the extent of Hey-binding to target promoters, subsequent Hdac recruitment and lower histone acetylation. Functionally, treatment with the Hdac inhibitor TSA abolished Hey target gene regulation. However, in CM the repressive effect of Hey-binding is lost for a subset of genes. These lack Hey-dependent histone deacetylation in CM and are enriched for binding sites of cardiac specific activators like Srf, Nkx2-5, and Gata4. ES cells and cardiomyocytes with Hey1 or Hey2 overexpression were compared to control cells
Project description:We report the identification of genomic regions bound by RBP2 and JARID2 in mouse cardiomyocytes. RBP2 generates methylated lysine 4 in histone H3. Consistent with previous data, RBP2 binds at the TSS regions. However, we found that overepresentation of gene ontologies (GO) for RBP2 targets in cardiomyocytes is drastically different from those in mouse embryonic stem (ES) cells. In cardiomyocytes, there is overepresentation of genes involved in heart morphogenesis and vasculogenesis. Strikingly, we found that location of JARID2, a factor critical for ES cell function, significantly overlaps with RBP2 location in cardiomyocytes.