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Tip60-mediated H2A.Z acetylation is required for neuronal fate specification and bivalent gene activation [RNA-Seq]

ABSTRACT: Examination of the effects of Tip60/Kat5 depletion on gene expression dynamics during Ascl1-mediated direct reprogramming of mouse embryonic fibroblasts (MEFs) into induced neuronal cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE181887 | GEO | 2022/11/22

REPOSITORIES: GEO

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Tip60-mediated H2A.Z acetylation is required for neuronal fate specification and bivalent gene activation [ATAC-Seq]

Project description:Examination of the effects of Tip60/Kat5 depletion on chromatin accessibility dynamics during Ascl1-mediated direct reprogramming of mouse embryonic fibroblasts (MEFs) into induced neuronal cells.

2022-11-22 | GSE181964 | GEO

Tip60-mediated H2A.Z acetylation is required for neuronal fate specification and bivalent gene activation [Cut & Tag]

Project description:Tip60-dependnet histone modification/occupancy dynamics during Ascl1-mediated direct reprogramming of mouse embryonic fibroblasts (MEFs) into induced neuronal cells.

2022-11-22 | GSE181888 | GEO

Tip60-mediated H2A.Z acetylation promotes neuronal fate specification and bivalent gene activation.

Project description:Cell lineage specification is accomplished by a concerted action of chromatin remodeling and tissue-specific transcription factors. However, the mechanisms that induce and maintain appropriate lineage-specific gene expression remain elusive. Here, we used an unbiased proteomics approach to characterize chromatin regulators that mediate the induction of neuronal cell fate. We found that Tip60 acetyltransferase is essential to establish neuronal cell identity partly via acetylation of the histone variant H2A.Z. Despite its tight correlation with gene expression and active chromatin, loss of H2A.Z acetylation had little effect on chromatin accessibility or transcription. Instead, loss of Tip60 and acetyl-H2A.Z interfered with H3K4me3 deposition and activation of a unique subset of silent, lineage-restricted genes characterized by a bivalent chromatin configuration at their promoters. Altogether, our results illuminate the mechanisms underlying bivalent chromatin activation and reveal that H2A.Z acetylation regulates neuronal fate specification by establishing epigenetic competence for bivalent gene activation and cell lineage transition.

| S-EPMC9779922 | biostudies-literature

RNA-sequencing data of Tip60 deleted and control mouse embryonic fibrobasts

Project description:In this study we examined the effects of loss of the MYST histone acetyltransferase TIP60 (KAT5) in mouse embryonic fibroblasts (MEFs), human embryonic kidney cells 293 (HEK293), and human osteosarcoma cells (U2OS) on cell proliferation, BrdU incorporation, cell cycle progression, apoptotic and other forms of cell death, DNA damage, histone acetylation at specific lysine residues and RNA expression levels. This dataset relates to MEFs. To assess the effects of loss of TIP60 on RNA levels, RNA-seq was performed on MEFs, where the TIP60 gene was deleted using Cre/loxP technology. Nuclear translocation was induced with 4-OH-tamoxifen treatment for 3 and 5 days to induce TIP60 gene deletion in the samples also containing the loxP sited in the Tip60 locus.

2022-07-22 | GSE208380 | GEO

Tip60-mediated H2A.Z acetylation promotes neuronal fate specification and bivalent gene activation.

Project description:Tip60-mediated H2A.Z acetylation promotes neuronal fate specification and bivalent gene activation.

| PRJNA754094 | ENA

Tip60-mediated H2A.Z acetylation promotes neuronal fate specification and bivalent gene activation.

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

2022-11-22 | GSE181965 | GEO

RNA-sequencing data of TIP60 mutated and control U2OS cells

Project description:In this study we examined the effects of loss of the MYST histone acetyltransferase TIP60 (KAT5) in mouse embryonic fibroblasts (MEFs), human embryonic kidney cells 293 (HEK293), and human osteosarcoma cells (U2OS) on cell proliferation, BrdU incorporation, cell cycle progression, apoptotic and other forms of cell death, DNA damage, histone acetylation at specific lysine residues and RNA expression levels. This dataset relates to U2OS cells. To assess the effects of loss of TIP60 on RNA levels, RNA-seq was performed on U2OS cells, where the TIP60 gene was mutated by CRISPR/Cas9 technology using single guide RNA #1 (g1/C9), single guide RNA #2 (g2/C9), or guide-only controls (g1 or g2). The expression of the guide RNA was induced with doxycycline treatment for 4 days to induce TIP60 gene mutation in the samples also expressing the Cas9 enzyme.

2022-07-22 | GSE208382 | GEO

RNA-sequencing data of TIP60 mutated and control HEK293 cells

Project description:In this study we examined the effects of loss of the MYST histone acetyltransferase TIP60 (KAT5) in mouse embryonic fibroblasts (MEFs), human embryonic kidney cells 293 (HEK293), and human osteosarcoma cells (U2OS) on cell proliferation, BrdU incorporation, cell cycle progression, apoptotic and other forms of cell death, DNA damage, histone acetylation at specific lysine residues and RNA expression levels. This dataset relates to HEK293 cells. To assess the effects of loss of TIP60 on RNA levels, RNA-seq was performed on HEK293 cells, where the TIP60 gene was mutated by CRISPR/Cas9 technology using single guide RNA #1 (g1/C9), single guide RNA #2 (g2/C9), or guide-only controls (g1 or g2). The expression of the guide RNA was induced with doxycycline treatment for 3 days to induce TIP60 gene mutation in the samples also expressing the Cas9 enzyme.

2022-07-22 | GSE208379 | GEO

Hdac6 regulates Tip60-p400 function in stem cells (sequencing)

Project description:The Tip60 (also known as Kat5) lysine acetyltransferase functions broadly as a transcriptional co-activator that acetylates histones. In contrast, Tip60 functions in embryonic stem cells (ESCs) both to silence genes that promote differentiation and to activate genes required for proliferation. The mechanism by which Tip60 functions as a repressor is unknown. Here we show that the class II histone deacetylase Hdac6 co-purifies with Tip60-p400 complex from ESCs and is necessary for complete silencing of most differentiation genes targeted by Tip60. In contrast to differentiated cells, where Hdac6 is mainly cytoplasmic and does not interact with Tip60, Hdac6 is largely nuclear in ESCs and neural stem cells (NSCs) and interacts with Tip60-p400 in both cell types. Hdac6 is enriched at promoters bound by Tip60-p400 in ESCs, but while Tip60 binds on both sides of transcription start sites (TSSs), Hdac6 binding overlaps with only the downstream Tip60 peak. Surprisingly, Hdac6 does not deacetylate histones at these sites, but rather is required for Tip60 binding. These data suggest that nuclear exclusion of Hdac6 during differentiation plays a major role in modulation of Tip60-p400 function. We determined the genome-wide localization of Tip60 and Hdac6 in mouse ES cells, and examined genomic binding profiles of Tip60 and Hdac6 upon indicated knockdown by ChIP-seq. We examined genomic binding profiles of p400 upon indicated knockdown by ChIP-seq.

2013-11-20 | E-GEOD-42209 | biostudies-arrayexpress

Tip60-mediated H2A.Z acetylation is required for neuronal fate specification and bivalent gene activation [Cut & Tag]

Project description:Tip60-mediated H2A.Z acetylation is required for neuronal fate specification and bivalent gene activation [Cut & Tag]

| PRJNA753812 | ENA