Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA260926 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1574330_1.fastq.gz | Fastqsanger.gz | |||
| SRR1574330_2.fastq.gz | Fastqsanger.gz | |||
| SRR1574331_1.fastq.gz | Fastqsanger.gz | |||
| SRR1574331_2.fastq.gz | Fastqsanger.gz | |||
| SRR1574332_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:MEF2D drives photoreceptor development through a genome-wide competition for tissue-specific enhancers
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Project description:MEF2D drives photoreceptor development through a genome-wide competition for tissue-specific enhancers (ChIP-Seq)
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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 | GSE61391 | GEO
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
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.
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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.
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Project description:Transcriptional enhancers are the primary determinants of tissue-specific gene expression and influence a variety of cellular phenotypes. The regulatory components controlling enhancer assembly and turnover during stem cell development remain largely unknown. Here we compared the similarities and differences in enhancer landscape, transcriptional factor (TF) occupancy and transcriptomic changes in human primary fetal and adult hematopoietic stem/progenitor cells (HSPCs) and committed erythroid progenitors. We find that enhancers are modulated dynamically and extensively, and direct lineage and developmental stage-specific transcriptional programs. GATA2-to-GATA1 switch is prevalent within transcriptionally dynamic enhancers and drives enhancer commissioning. Further examination of lineage-specific enhancers identified TFs and their combinatorial patterns with known and unknown roles as putative drivers of enhancer turnover during differentiation. Importantly, by site-directed loss-of-function analysis of individual lineage-selective enhancers within the SLC25A37 super-enhancer using CRISPR/Cas9-mediated genomic editing, we uncover unexpected functional hierarchy of constituent enhancers within the super-enhancer cluster. Despite the indistinguishable chromatin features between the GATA switch enhancers at the GATA2 gene, we reveal through genomic editing the functional diversity of GATA switch enhancers in which enhancers with opposing functions cooperate to coordinate gene expression during development. Thus, genome-wide enhancer profiling coupled with in-depth enhancer editing in situ provide critical insights into the functional hierarchy and complexity of enhancers during stem cell development.
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Project description:Group 2 innate lymphoid cells (ILC2s) orchestrate tissue homeostasis, allergic disorders and anti-helminth protective immunity through their production of cytokines. However, their rarity has hampered high-throughput genetic screening approaches to uncover novel ILC2 regulators in an unbiased manner. We combined expansion of progenitors from multi-reporter mouse strains with optimised ILC differentiation cultures to perform CRISPR-Cas9 screens for regulators of ILC2 development and function. Mef2d emerged as a critical regulator of GATA3 and IL-13, and was essential for type-2 immunity as demonstrated by conditional Mef2d-deficient mice, including a Boolean-ILC2-Cre (BIC) mouse strain developed to enable ILC2-specific gene deletion. Mechanistically, Mef2d bound and transcriptionally repressed the Zc3h12a locus encoding the endonuclease Regnase-1, a negative regulator of IL-33 receptor (ST2) and GATA3 expression, thereby promoting IL-33-mediated ILC2 proliferation and cytokine production. Notably, in ILC2s Mef2d also acted downstream of leukotriene C4-induced calcium-mediated signalling to translocate NFAT1 to the nucleus to promote type-2 gene transcription. These Mef2d-mediated pathways converge and feedback to potentiate type-2 immunity.
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Project description:Group 2 innate lymphoid cells (ILC2s) orchestrate tissue homeostasis, allergic disorders and anti-helminth protective immunity through their production of cytokines. However, their rarity has hampered high-throughput genetic screening approaches to uncover novel ILC2 regulators in an unbiased manner. We combined expansion of progenitors from multi-reporter mouse strains with optimised ILC differentiation cultures to perform CRISPR-Cas9 screens for regulators of ILC2 development and function. Mef2d emerged as a critical regulator of GATA3 and IL-13, and was essential for type-2 immunity as demonstrated by conditional Mef2d-deficient mice, including a Boolean-ILC2-Cre (BIC) mouse strain developed to enable ILC2-specific gene deletion. Mechanistically, Mef2d bound and transcriptionally repressed the Zc3h12a locus encoding the endonuclease Regnase-1, a negative regulator of IL-33 receptor (ST2) and GATA3 expression, thereby promoting IL-33-mediated ILC2 proliferation and cytokine production. Notably, in ILC2s Mef2d also acted downstream of leukotriene C4-induced calcium-mediated signalling to translocate NFAT1 to the nucleus to promote type-2 gene transcription. These Mef2d-mediated pathways converge and feedback to potentiate type-2 immunity.
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Project description:Group 2 innate lymphoid cells (ILC2s) orchestrate tissue homeostasis, allergic disorders and anti-helminth protective immunity through their production of cytokines. However, their rarity has hampered high-throughput genetic screening approaches to uncover novel ILC2 regulators in an unbiased manner. We combined expansion of progenitors from multi-reporter mouse strains with optimised ILC differentiation cultures to perform CRISPR-Cas9 screens for regulators of ILC2 development and function. Mef2d emerged as a critical regulator of GATA3 and IL-13, and was essential for type-2 immunity as demonstrated by conditional Mef2d-deficient mice, including a Boolean-ILC2-Cre (BIC) mouse strain developed to enable ILC2-specific gene deletion. Mechanistically, Mef2d bound and transcriptionally repressed the Zc3h12a locus encoding the endonuclease Regnase-1, a negative regulator of IL-33 receptor (ST2) and GATA3 expression, thereby promoting IL-33-mediated ILC2 proliferation and cytokine production. Notably, in ILC2s Mef2d also acted downstream of leukotriene C4-induced calcium-mediated signalling to translocate NFAT1 to the nucleus to promote type-2 gene transcription. These Mef2d-mediated pathways converge and feedback to potentiate type-2 immunity.
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