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KMT2B is selectively required for neuronal transdifferentiation

ABSTRACT: KMT2B is selectively required for neuronal transdifferentiation

PROVIDER: PRJNA493074 | ENA |

REPOSITORIES: ENA

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KMT2B is selectively required for neuronal transdifferentiation [RNAseq]

Project description:KMT2B is selectively required for neuronal transdifferentiation [RNAseq]

| PRJNA493076 | ENA

KMT2B is selectively required for neuronal transdifferentiation [ChIP-seq]

Project description:Transdifferentiation of fibroblasts into induced Neuronal cells (iNs) by neuronal-specific transcription factors Brn2, Myt1l and Ascl1 is a paradigmatic example of inter-lineage conversion across epigenetically distant cells. Despite tremendous progress on the transcriptional hierarchy underlying transdifferentiation, the enablers of the concomitant epigenome resetting remain to be elucidated. Here we investigated the role of KMT2A and KMT2B, two histone H3 lysine 4 methylases with cardinal roles in development, through individual and combined inactivation. We found that Kmt2b, whose human homologue’s mutations cause dystonia, is selectively required for iN conversion through the suppression of the alternative myocyte program and the induction of neuronal maturation genes.

2018-09-29 | GSE120635 | GEO

KMT2B is selectively required for neuronal transdifferentiation [RNAseq]

2018-09-26 | GSE120440 | GEO

KMT2B is selectively required for neuronal transdifferentiation [ChIP-seq]

Project description:KMT2B is selectively required for neuronal transdifferentiation [ChIP-seq]

| PRJNA493814 | ENA

KMT2B is selectively required for neuronal transdifferentiation

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

2018-09-26 | GSE120441 | GEO

KMT2B Is Selectively Required for Neuronal Transdifferentiation, and Its Loss Exposes Dystonia Candidate Genes.

Project description: Not available

| S-EPMC6218204 | biostudies-literature

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.

2019-01-26 | GSE125694 | GEO

Oct1 and OCA-B are Selectively Required for CD4 Memory T Cell Formation and Function (ChIP-seq)

Project description:Epigenetic changes are crucial for the generation of immunological memory. Failure to generate or maintain these changes will result in poor memory responses. Similarly, augmenting or stabilizing the correct epigenetic states offers a potential method of enhancing immune memory. Yet the transcription factors that regulate these processes are poorly defined, as are the target genes they control and they chromatin-modifying complexes they recruit. Using model pathogens and three different mouse models, we find that the widely expressed transcription factor Oct1 and its cofactor OCA-B are selectively required for the in vivo generation of functional CD4 memory. In vitro, both proteins are required to maintain a poised state at the Il2 target locus in resting but previously stimulated CD4 T cells, and to generate robust Il2 expression upon restimulation. Gene expression profiling indicates that OCA-B is also required for the robust re-expression of multiple other targets including Ifng and Il17a. ChIPseq identify multiple differentially expressed direct targets. We identify an underlying mechanism involving OCA-B recruitment of the histone lysine demethylase Jmjd1a to targets such as Il2 and Ifng. The findings pinpoint Oct1 and OCA-B as unanticipated mediators of CD4 T cell memory. Examination of transcription factor occupancy in CD4 T cells upon rest and restimulation.

2015-09-17 | E-GEOD-65918 | biostudies-arrayexpress

Oct1/Pou2f1 is selectively required for gut regeneration and regulates gut malignancy

Project description:Oct1/Pou2f1 is selectively required for gut regeneration and regulates gut malignancy

| PRJNA509072 | ENA

Comparative transcriptomics of B cell transdifferentiation in human and mouse. ChIP-Seq data

Project description:Exogenous overexpression of CEBPA transcription factor induces transdifferentiation from pro B cells into functional macrophages. Here we report the CEBPA binding ChIP-Seq data at 12 hours time point after induction of transdifferentiation in human BLaER1 cells (Rapino et al. 2013).

2022-01-01 | E-MTAB-7114 | biostudies-arrayexpress

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