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Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [H3K9 ChIP-seq]

ABSTRACT: Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [H3K9 ChIP-seq]

PROVIDER: PRJNA1064906 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27553147_1.fastq.gz	Fastqsanger.gz
	SRR27553147_2.fastq.gz	Fastqsanger.gz
	SRR27553148_1.fastq.gz	Fastqsanger.gz
	SRR27553148_2.fastq.gz	Fastqsanger.gz
	SRR27553149_1.fastq.gz	Fastqsanger.gz

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Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [H3K9 ChIP-seq]

Project description:Members of the Myt (myelin transcription factor) family have been implicated in neuronal development. However, their in vivo roles in OL lineage development have not been systematically investigated. Here, we identified Myt1 transcription factor as a crucial regulator of oligodendrocyte differentiation in the developing central nervous system. Conventional knockout of Myt1 causes a remarkable delay in the initiation of OL differentiation, without affecting the generation and proliferation of OPCs. Conversely, hyperactivation of Myt1 induces precocious OL differentiation both in vitro and in vivo. Using a combination of RNA-seq and ChIP-seq analyses, we identified Nkx2.2 as a key target of Myt1 to switch on the OL differentiation program. Mechanistically, specific binding of Myt1 in the Nkx2.2 gene loci inhibits the nucleosomal histone deacetylation via hindering the HDAC1 repressor complex integrity and reducing the deacetylation activity of HDAC1. Additionally, we demonstrated that Myt1 functions downstream of Notch signaling pathway in controlling the timing of OL differentiation. Collectively, our data demonstrate that Myt1 is a major regulator of OL differentiation and provide insight into the epigenetic regulatory mechanisms under OL development. Myt1 is, therefore, a promising therapeutic target for enhancing the OL differentiation and myelination/remyelination during development or after demyelination insults.

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Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [RNA-seq]

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Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [ATAC-seq]

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Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [MYT ChIP-seq]

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Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation

Project description:Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation

| PRJNA1064900 | ENA

Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [ATAC-seq]

Project description:Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [ATAC-seq]

| PRJNA1065891 | ENA

Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [RNA-seq]

Project description:Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [RNA-seq]

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Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [MYT ChIP-seq]

Project description:Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [MYT ChIP-seq]

| PRJNA1064907 | ENA

A Myt1 family transcription factor defines neuronal fate by repressing non-neuronal genes

Project description:Cellular differentiation requires both activation of target cell programs and repression of non-target cell programs. Transcriptional repressors such as RE1-silencing transcription factor (REST) and Hairy/Enhancer of Split (Hes) repress neuronal genes in non-neuronal cells. However, it is unknown whether transcriptional repressors of non-neuronal genes in neuronal precursors are required to specify neuronal fate during development. The Myt1 family of zinc finger transcription factors contributes to fibroblast to neuron reprogramming in vitro by repressing Notch signaling. Here, we show that ztf-11 (Zinc-finger Transcription Factor-11), the sole Caenorhabditis elegans Myt1 homolog, is required for neurogenesis in multiple neuronal lineages, including an in vivo developmental epithelial-to-neuronal transdifferentiation event. ztf-11 is exclusively expressed in all neuronal precursors with remarkable specificity at single cell resolution. Loss of ztf-11 leads to upregulation of non-neuronal genes and reduced neurogenesis. Ectopic expression of ztf-11 in epidermal lineages is sufficient to produce additional neurons. Our genetic and genomic experiments show that ZTF-11 indeed functions as a transcriptional repressor to suppress the activation of non-neuronal genes in neurons; however, it does not function via repression of Notch signaling. Instead, ZTF-11 binds to the MuvBco-repressor complex, which we show is also required for neurogenesis. These results dovetail with ability of Myt1l (Myt1-like) to drive neuronal transdifferentiation in vitro in vertebrate systems. Together, we identified an evolutionarily conserved mechanism to specify neuronal cell fate by repressing non-neuronal genes.

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Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-10-01 | GSE253257 | GEO