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Mus musculus

ABSTRACT: MEF2D drives photoreceptor development through a genome-wide competition for tissue-specific enhancers (ChIP-Seq)

PROVIDER: PRJNA260927 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1574490.fastq.gz	Fastqsanger.gz
	SRR1574500.fastq.gz	Fastqsanger.gz
	SRR1574510.fastq.gz	Fastqsanger.gz
	SRR1574491.fastq.gz	Fastqsanger.gz
	SRR1574501.fastq.gz	Fastqsanger.gz

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MEF2D drives photoreceptor development through a genome-wide competition for tissue-specific enhancers

Project description:MEF2D drives photoreceptor development through a genome-wide competition for tissue-specific enhancers

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Mus musculus

Project description:MEF2D drives photoreceptor development through a genome-wide competition for tissue-specific enhancers (RNA-Seq)

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MEF2D drives photoreceptor development through a genome-wide competition for tissue-specific enhancers (RNA-Seq)

Project description:Organismal development requires the precise coordination of genetic programs to regulate cell fate and function. MEF2 transcription factors play essential roles in this process but how these broadly expressed factors contribute to the generation of specific cell types during development is poorly understood. Here we show that despite being expressed in virtually all mammalian tissues, in the retina MEF2D binds to retina-specific enhancers and controls photoreceptor cell development. MEF2D achieves specificity by cooperating with a retina-specific factor CRX, which recruits MEF2D away from canonical MEF2 binding sites, and redirects it to retina-specific enhancers that lack the consensus MEF2 sequence. Once bound to retina-specific enhancers, MEF2D and CRX co-activate the expression of photoreceptor-specific genes that are critical for retinal function. These findings demonstrate that broadly expressed TFs acquire specific functions through competitive recruitment to enhancers by tissue-specific TFs, and through cooperative activation of these enhancers to regulate tissue-specific genes.

2015-03-19 | GSE61389 | GEO

MEF2D drives photoreceptor development through a genome-wide competition for tissue-specific enhancers (ChIP-Seq)

2015-03-19 | GSE61391 | GEO

Different class IIa HDACs repressive complexes regulate specific epigenetic responses related to cell survival in leiomyosarcoma cells

Project description:Purpose: Define the transcriptional networks supervising class IIa HDAC expression. Outcome: We demonstrate that MEF2D is the key factor controlling HDAC9 transcription. Comprehensive genome-wide studies demonstrate that HDAC4 and HDAC9 supervise different genetic programs and show both specific and common genomic bindings. Although the number of MEF2-target genes commonly regulated is similar, only HDAC4 represses many additional genes that are not MEF2D targets. HDAC4-/- and HDAC9-/- cells increase H3K27ac levels around the TSS of the respective repressed genes. However, these genes rarely show bindings of the HDACs at their promoters. Frequently HDAC4 and HDAC9 bind intergenic regions. We demonstrate that these regions, recognized by MEF2D/HDAC4/HDAC9 repressive complexes, show the features of active enhancers.

2019-11-13 | GSE132569 | GEO

Different class IIa HDACs repressive complexes regulate specific epigenetic responses related to cell survival in leiomyosarcoma cells.

2019-11-12 | GSE132622 | GEO

Mus musculus

Project description:ChIP-seq Accurately Predicts Tissue-Specific Activity of Enhancers

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Alternate exon switching establishes a tissue-specific transcription factor to mediate temporal activation of gene expression during differentiation

Project description:Although splicing occurs in most multi-exon genes, the generation of distinct isoforms through the alternate use of mutually exclusive exons is less prevalent. As exon-switching events have the potential to give rise to isoforms with different cellular functions, we have explored the role of the muscle-specific (Mef2Da2) and ubiquitously expressed (Mef2Da1) isoforms of the transcription factor Mef2D in myogenesis. Here we show that both isoforms of Mef2D bind a largely overlapping subset of genomic loci, yet only the muscle-specific Mef2Da2 isoform can activate the late myogenic gene expression program. This differential ability to activate transcription is modulated by PKA signaling where Mef2Da1 is efficiently phosphorylated by the kinase to enhance its association with repressive HDAC-deacetylase complexes. In contrast, alternate exon usage in Mef2Da2 renders the protein resistant to PKA phosphorylation, allowing it to interact with transcriptionally permissive Ash2L-trithorax complex. Our findings support a model wherein alternative exon usage allows Mef2D to transition from a repressor to activator in a myogenic environment rich in PKA activity. Thus we have identified a novel paradigm in which a ubiquitously expressed transcription factor has evolved to undergo tissue-specific alternative exon usage to permit the proper temporal activation of a gene expression program during differentiation. ChIP-Seq profiling of Mef2Da1 and Mef2Da2 isoforms generated by alternate splicing

2013-06-01 | E-GEOD-43223 | biostudies-arrayexpress

ChIP-seq Identification of Weakly Conserved Heart Enhancers

Project description:Accurate control of tissue-specific gene expression plays a pivotal role in heart development. However, few cardiac transcriptional enhancers have thus far been identified. Extreme non-coding sequence conservation successfully predicts enhancers active in many tissues, but fails to identify substantial numbers of enhancers active in the heart. We used ChIP-seq with the enhancer-associated protein p300 from mouse embryonic heart tissue to identify over three thousand candidate heart enhancers genome-wide. In contrast to other studied tissues at this time-point, most candidate heart enhancers are not deeply conserved in vertebrate evolution. Nevertheless, the testing of 130 candidate regions in a transgenic mouse assay revealed that most of them reproducibly function as enhancers active in the heart, irrespective of their degree of evolutionary constraint. These results provide evidence for tissue-dependent differences in evolutionary constraint of enhancers acting through the transcriptional co-activator p300 at this time-point, and identify a large population of poorly conserved heart enhancers. Examination of p300 binding in embryonic stage 11.5 mouse heart and midbrain

2010-08-22 | E-GEOD-22549 | biostudies-arrayexpress

Project description:Mef2D ChIP-seq

| PRJNA887931 | ENA