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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Rattus norvegicus

PROVIDER: GSE253257 | GEO | 2024/10/01

REPOSITORIES: GEO

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

2024-10-01 | GSE253491 | GEO

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

2024-10-01 | GSE253256 | GEO

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

2024-10-01 | GSE253255 | GEO

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

2024-10-01 | GSE253254 | GEO

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 [RNA-seq]

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

| PRJNA1064910 | 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 [H3K9 ChIP-seq]

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

| PRJNA1064906 | ENA

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

The novel BTB/POZ and zinc finger factor Zbtb45 is essential for proper glial differentiation of neural and oligodendrocyte progenitor cells.

Project description:Understanding the regulatory mechanisms controlling the fate decisions of neural stem cells (NSCs) is a crucial issue to shed new light on mammalian central nervous system (CNS) development in health and disease. We have investigated a possible role for the previously uncharacterized BTB/POZ-domain containing zinc finger factor Zbtb45 in the differentiation of NSCs and postnatal oligodendrocyte precursors. In situ hybridization histochemistry and RT-qPCR analysis revealed that Zbtb45 mRNA was ubiquitously expressed in the developing CNS in mouse embryos at embryonic day (E) 12.5 and 14.5. Zbtb45 mRNA knockdown in embryonic forebrain NSCs by siRNA resulted in a rapid decrease in the expression of oligodendrocyte-characteristic genes after mitogen (FGF2) withdrawal, whereas the expression of astrocyte-associated genes such as CD44 and GFAP increased compared to control. Accordingly, the number of astrocytes was significantly increased seven days after Zbtb45 siRNA delivery to NSCs, in contrast to the numbers of neuronal and oligodendrocyte-like cells. Surprisingly, mRNA knockdown of the Zbtb45-associated factor Med31, a subunit of the Mediator complex, did not result in any detectable effect on NSC differentiation. Similar to NSCs, Zbtb45 mRNA knockdown in oligodendrocyte precursors (CG-4) reduced oligodendrocyte maturation upon mitogen withdrawal associated with down-regulation of the mRNA expression and protein levels of markers for oligodendrocytic differentiation. Zbtb45 mRNA knockdown did not significantly affect proliferation or cell death in any of the cell types. Based on these observations, we propose that Zbtb45 is a novel regulator of glial differentiation.

| S-EPMC3047810 | biostudies-literature

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