| Experiment Id | GSE77588 | Name | CTCF counter-regulates cardiomyocyte development and maturation programs in the embryonic heart [RNA-seq] |
| Experiment Type | RNA-Seq | Study Type | WT vs. Mutant |
| Source | GEO | Curation Date | 2022-04-26 |
| description | Analysis of chromatin architecture suggests that the 3D structure of the genome plays a major role in regulating gene expression, orchestrating the compartmentalization of chromatin and facilitating specific enhancer-promoter interactions. However, the mechanisms that control this structuring of the genome are not fully understood. We have addressed this issue by analyzing the role of CTCF, a major architectural factor in chromatin structure, in the embryonic heart. Loss of CTCF triggered an overall downregulation of the cardiac developmental program, suggesting that CTCF facilitates enhancer-promoter interactions in the developing heart. Detailed analysis of the IrxA gene cluster showed that CTCF loss leads to disruption of the heart-specific regulatory domain that surrounds Irx4, resulting in changes in expression of IrxA cluster genes and neighboring genes. In contrast to the critical role proposed for CTCF in organizing large-scale chromatin domains, our results show that CTCF preferentially mediates local regulatory interactions. RNAseq of mouse embryonic E10.5 hearts in three conditions: 1) control (labeled as WT), 2) heterozygous (labeled as HET) and 3) homozygous (labeled as KO). Three replicates were performed for each condition, each consisting of a pool of 6 hearts. Tissue was mechanically disaggregated and RNA extracted with trizol and purified through columns. |
