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H3 acetylation selectively promotes basal progenitor proliferation and neocortex expansion by activating TRNP1 expression

ABSTRACT: We performed RNA-Seq and H3K9ac ChIP-Seq from the whole embryonic cortex at E15.5 from BAF155 cKO mice treated either with vehicle or HDAC inhibitor (TSA).

ORGANISM(S): Mus musculus

PROVIDER: GSE176194 | GEO | 2021/06/05

REPOSITORIES: GEO

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H3 acetylation selectively promotes basal progenitor proliferation and neocortex expansion.

Project description:Increase in the size of human neocortex―acquired in evolution―accounts for the unique cognitive capacity of humans. This expansion reflects the evolutionarily enhanced proliferative ability of basal progenitors (BPs), including the basal radial glia and basal intermediate progenitors (bIPs) in mammalian cortex, which may have been acquired through epigenetic alterations in BPs. However, how the epigenome in BPs differs across species is not known. Here, we report that histone H3 acetylation is a key epigenetic regulation in bIP amplification and cortical expansion. Through epigenetic profiling of sorted bIPs, we show that histone H3 lysine 9 acetylation (H3K9ac) is low in murine bIPs and high in human bIPs. Elevated H3K9ac preferentially increases bIP proliferation, increasing the size and folding of the normally smooth mouse neocortex. H3K9ac drives bIP amplification by increasing expression of the evolutionarily regulated gene, Trnp1, in developing cortex. Our findings demonstrate a previously unknown mechanism that controls cortical architecture.

| S-EPMC8443185 | biostudies-literature

Chromatin remodeling BAF155 subunit regulates the genesis of basal progenitors in developing cortex

Project description:We have analyzed gene expression differences between control, BAF155 conditional knockout (cKO) and Pax6 cKO embryonic cortices at E15.5.

2018-05-11 | GSE114351 | GEO

H3 acetylation selectively promotes basal progenitor proliferation and neocortex expansion by activating TRNP1 expression

Project description:H3 acetylation selectively promotes basal progenitor proliferation and neocortex expansion by activating TRNP1 expression

| PRJNA735244 | ENA

Requisite chromatin remodeling for myeloid and erythroid lineage differentiation from erythromyeloid progenitors

Project description:The mammalian SWI/SNF chromatin-remodeling BAF (BRG1/BRM associated factor) complex plays an essential role in developmental and pathological processes. We show that the deletion of Baf155 encoding a subunit of BAF complex in the Tie2(+) lineage (Baf155 CKO) leads to defects in the yolk sac myeloid and definitive erythroid (EryD) lineage differentiation from erythromyeloid progenitors (EMPs) and embryonic lethality. Baf155 knock-down in EMP was sufficient to block myeloid and EryD differentiation. Chromatin of the myeloid gene loci in Baf155 CKO EMPs was largely inaccessible and was enriched mostly by the ETS binding motif. BAF155 interacted with PU.1 and was recruited to the PU.1 in target gene loci together with p300 and KDM6a. Treatment of Baf155 CKO embryos with GSK126, an inhibitor of the H3K27me2/3 methyltransferase EZH2, rescued myeloid lineage gene expression. These studies uncover the indispensable BAF mediated chromatin remodeling of the myeloid gene loci at the EMP stage.

2021-03-08 | GSE159381 | GEO

Requisite chromatin remodeling for myeloid and erythroid lineage differentiation from erythromyeloid progenitors

Project description:The mammalian SWI/SNF chromatin-remodeling BAF (BRG1/BRM-associated factor) complex has an essential role in developmental and pathological processes. We show that deletion of Baf155 encoding a subunit of the BAF complex in the Tie2(+) lineage (Baf155 CKO) leads to defects in yolk sac myeloid and definitive erythroid (EryD) lineage differentiation from erythromyeloid progenitors (EMPs). The chromatin of myeloid gene loci in Baf155 CKO EMPs is mostly inaccessible and enriched mainly by the ETS binding motif. BAF155 interacts with PU.1 and is recruited to PU.1 target gene loci together with p300 and KDM6a. Treatment of Baf155 CKO embryos with GSK126, an H3K27me2/3 methyltransferase EZH2 inhibitor, rescues myeloid lineage gene expression. This study uncovers indispensable BAF-mediated chromatin remodeling of myeloid gene loci at the EMP stage. Future studies exploiting epigenetics in generation and application of EMP derivatives for tissue repair, regeneration, and disease are warranted.

2020-11-17 | GSE144243 | GEO

H3 Acetylation-Induced Basal Progenitor Generation and Neocortex Expansion Depends on the Transcription Factor Pax6.

Project description:Enrichment of basal progenitors (BPs) in the developing neocortex is a central driver of cortical enlargement. The transcription factor Pax6 is known as an essential regulator in generation of BPs. H3 lysine 9 acetylation (H3K9ac) has emerged as a crucial epigenetic mechanism that activates the gene expression program required for BP pool amplification. In this current work, we applied immunohistochemistry, RNA sequencing, chromatin immunoprecipitation and sequencing, and the yeast two-hybrid assay to reveal that the BP-genic effect of H3 acetylation is dependent on Pax6 functionality in the developing mouse cortex. In the presence of Pax6, increased H3 acetylation caused BP pool expansion, leading to enhanced neurogenesis, which evoked expansion and quasi-convolution of the mouse neocortex. Interestingly, H3 acetylation activation exacerbates the BP depletion and corticogenesis reduction effect of Pax6 ablation in cortex-specific Pax6 mutants. Furthermore, we found that H3K9 acetyltransferase KAT2A/GCN5 interacts with Pax6 and potentiates Pax6-dependent transcriptional activity. This explains a genome-wide lack of H3K9ac, especially in the promoter regions of BP-genic genes, in the Pax6 mutant cortex. Together, these findings reveal a mechanistic coupling of H3 acetylation and Pax6 in orchestrating BP production and cortical expansion through the promotion of a BP gene expression program during cortical development.

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Histone methyltransferase SETDB1 selectively regulates cortical HTR3A interneuron development and anxiety-like behavior in mice

Project description:Histone methyltransferase SETDB1 is critically involved in brain development, but its role in regulating GABAergic interneurons remains unknown. Here, we used RNA-seq and ATAC-seq to study the gene expression and chromatin accessibility in ganglionic eminences (GE) at E15.5 from brain-specific Setdb1 conditional knockout mice (Setdb1-Nestin-cKO) and controls both in vitro and in vivo.

2022-12-31 | GSE186806 | GEO

Histone methyltransferase SETDB1 selectively regulates cortical HTR3A interneuron development and anxiety-like behavior in mice [ChIP-seq]

Project description:SETDB1 functioning as a histone H3K9 specific methyltransferase, is critically involved in brain development. Here, we used H3K9me3 and H3K27me3 ChIPseq to study H3K9me3 redistribution and defined enhancer function of elements in genomes of NPCs from ganglionic eminences (GE) in brain-specific Setdb1 conditional knockout mice (Setdb1-Nestin-cKO) and controls at E15.5.

2023-05-18 | GSE200726 | GEO

Acetylation on Histone H3 Lysine 9 Mediates a Switch from Transcription Initiation to Elongation

Project description:The transition from transcription initiation to elongation is a key regulatory step in gene expression, which requires RNA polymerase II (Pol II) to escape promoter proximal pausing on chromatin. While elongation factors promote pause release leading to transcription elongation, the role of epigenetic modifications during this critical transition step is poorly understood. Two histone marks on histone H3, lysine 4 trimethylation (H3K4me3) and lysine 9 acetylation (H3K9ac), co-localize on active gene promoters and are associated with active transcription. H3K4me3 can promote transcription initiation, yet the functional role of H3K9ac is much less understood. We hypothesized that H3K9ac may function downstream of transcription initiation by recruiting specific proteins important for the next step of transcription. Here, we describe a functional role for H3K9ac in promoting Pol II pause release by directly recruiting the super elongation complex (SEC) to chromatin. H3K9ac serves as a substrate for direct binding of the SEC, as does acetylation of histone H4 lysine 5 (H4K5ac), to a lesser extent. Furthermore, lysine 9 on histone H3 is necessary for maximal Pol II pause release through SEC action, and loss of H3K9ac increases the Pol II pausing index on a subset of genes in HeLa cells. At select gene promoters, loss of H3K9ac or depletion of the SEC reduces gene expression and increases paused Pol II occupancy. We therefore propose that an ordered histone code drives progression through the transcription cycle, providing new mechanistic insight that SEC recruitment to certain acetylated histones promotes the subsequent release of paused Pol II needed for transcription elongation.

2017-07-11 | GSE99998 | GEO

Genome-wide analysis of histone H3 lysine 9 acetylation in Populus trichocarpa under drought stress

Project description:We report on the genome-wide distribution pattern of histone H3 lysine 9 acetylation (H3K9ac) and the pattern’s association with whole genome expression profiles in Populus trichocarpa subjected to soil-water depletion. We identified a set of drought responsive genes whose expression is directly regulated by differential modification of H3K9ac.

2018-12-27 | GSE81047 | GEO

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