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Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues

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

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE263160 | GEO | 2024/04/26

REPOSITORIES: GEO

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Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues

Project description:Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues

| PRJNA1095990 | ENA

Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues: RNA-Seq Timecourse from Developing Drosophila Eye

Project description:Previous work in the developing Drosophila wing revealed that cell cycle genes are subject to two types of chromatin regulation. The majority of cell cycle genes exhibit a simple regulatory landscape, with promoters that remain accessible even after cell cycle exit. A few critical, rate-limiting cell cycle genes show a more complex and dynamic landscape, and enhancers near these genes show evidence of decomissioning after cell cycle exit has occurred. Here we address whether the findings made in the wing are applicable to other postmitotic tissues that persist for the lifetime of the animal: the eye and the brain. We find that these tissues show similar chromatin accessibility profiles at cell cycle genes, suggesting that these modes of regulation are shared across tissues and that multiple strategies support cell cycle gene repression in the postmitotic state. These include stable repression at the promoters of most cell cycle genes, combined with enhancer decommissioning at a few select, rate-limiting genes.

2024-04-26 | GSE262726 | GEO

Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues: ATAC-Seq Timecourse from Drosophila Eye and Brain

2024-04-26 | GSE263159 | GEO

Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues: RNA-Seq Timecourse from Developing Drosophila Eye

Project description:Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues: RNA-Seq Timecourse from Developing Drosophila Eye

| PRJNA1093061 | ENA

DLX1 and the NuRD complex cooperate in enhancer decommissioning and transcriptional repression.

Project description:In the developing subpallium, the fate decision between neurons and glia is driven by expression of Dlx1/2 or Olig1/2, respectively, two sets of transcription factors with a mutually repressive relationship. The mechanism by which Dlx1/2 repress progenitor and oligodendrocyte fate, while promoting transcription of genes needed for differentiation, is not fully understood. We identified a motif within DLX1 that binds RBBP4, a NuRD complex subunit. ChIP-seq studies of genomic occupancy of DLX1 and six different members of the NuRD complex show that DLX1 and NuRD colocalize to putative regulatory elements enriched near other transcription factor genes. Loss of Dlx1/2 leads to dysregulation of genome accessibility at putative regulatory elements near genes repressed by Dlx1/2, including Olig2. Consequently, heterozygosity of Dlx1/2 and Rbbp4 leads to an increase in the production of OLIG2+ cells. These findings highlight the importance of the interplay between transcription factors and chromatin remodelers in regulating cell-fate decisions.

| S-EPMC9245191 | biostudies-literature

Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues: ATAC-Seq Timecourse from Drosophila Eye and Brain

Project description:Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues: ATAC-Seq Timecourse from Drosophila Eye and Brain

| PRJNA1095999 | ENA

DLX1 and the NuRD complex cooperate in enhancer decommissioning and transcriptional repression

Project description:In the developing subpallium, the fate decision between neurons and glia is driven by expression of Dlx1/2 or Olig1/2 respectively, two sets of transcription factors (TFs) with a mutually repressive relationship. The mechanism by which Dlx1/2 repress progenitor and oligodendrocyte fate, while promoting transcription of genes needed for differentiation, is not fully understood. We identified a motif within DLX1 that binds RBBP4, a NuRD complex subunit. ChIP-seq studies of genomic occupancy of DLX1 and six different members of the NuRD complex show that DLX1 and NuRD colocalize to putative regulatory elements (pREs) enriched near other transcription factor genes. Loss of Dlx1/2 leads to dysregulation of genome accessibility at pREs near genes repressed by Dlx1/2, including Olig2. Consequently, heterozygosity of Dlx1/2 and Rbbp4 leads to an increase in the production of OLIG2+ cells. These findings highlight the importance of the interplay between TFs and chromatin remodelers in regulating cell fate decisions.

2022-06-01 | GSE194076 | GEO

Silencing of the EPHB3 tumor-suppressor gene in human colorectal cancer through decommissioning of a transcriptional enhancer.

Project description:The protein tyrosine kinase Ephrin type-B receptor 3 (EPHB3) counteracts tumor-cell dissemination by regulating intercellular adhesion and repulsion and acts as tumor/invasion suppressor in colorectal cancer. This protective mechanism frequently collapses at the adenoma-carcinoma transition due to EPHB3 transcriptional silencing. Here, we identify a transcriptional enhancer at the EPHB3 gene that integrates input from the intestinal stem-cell regulator achaete-scute family basic helix-loop-helix transcription factor 2 (ASCL2), Wnt/?-catenin, MAP kinase, and Notch signaling. EPHB3 enhancer activity is highly variable in colorectal carcinoma cells and precisely reflects EPHB3 expression states, suggesting that enhancer dysfunction underlies EPHB3 silencing. Interestingly, low Notch activity parallels reduced EPHB3 expression in colorectal carcinoma cell lines and poorly differentiated tumor-tissue specimens. Restoring Notch activity reestablished enhancer function and EPHB3 expression. Although essential for intestinal stem-cell maintenance and adenoma formation, Notch activity seems dispensable in colorectal carcinomas. Notch activation even promoted growth arrest and apoptosis of colorectal carcinoma cells, attenuated their self-renewal capacity in vitro, and blocked tumor growth in vivo. Higher levels of Notch activity also correlated with longer disease-free survival of colorectal cancer patients. In summary, our results uncover enhancer decommissioning as a mechanism for transcriptional silencing of the EPHB3 tumor suppressor and argue for an antitumorigenic function of Notch signaling in advanced colorectal cancer.

| S-EPMC3977263 | biostudies-literature

Enhancer decommissioning by LSD1 during embryonic stem cell differentiation.

Project description:Transcription factors and chromatin modifiers are important in the programming and reprogramming of cellular states during development. Transcription factors bind to enhancer elements and recruit coactivators and chromatin-modifying enzymes to facilitate transcription initiation. During differentiation a subset of these enhancers must be silenced, but the mechanisms underlying enhancer silencing are poorly understood. Here we show that the histone demethylase lysine-specific demethylase 1 (LSD1; ref. 5), which demethylates histone H3 on Lys?4 or Lys?9 (H3K4/K9), is essential in decommissioning enhancers during the differentiation of mouse embryonic stem cells (ESCs). LSD1 occupies enhancers of active genes that are critical for control of the state of ESCs. However, LSD1 is not essential for the maintenance of ESC identity. Instead, ESCs lacking LSD1 activity fail to differentiate fully, and ESC-specific enhancers fail to undergo the histone demethylation events associated with differentiation. At active enhancers, LSD1 is a component of the NuRD (nucleosome remodelling and histone deacetylase) complex, which contains additional subunits that are necessary for ESC differentiation. We propose that the LSD1-NuRD complex decommissions enhancers of the pluripotency program during differentiation, which is essential for the complete shutdown of the ESC gene expression program and the transition to new cell states.

| S-EPMC4144424 | biostudies-literature

Enhancer decommissioning imposes an epigenetic barrier to sensory hair cell regeneration.

Project description:Adult mammalian tissues such as heart, brain, retina, and the sensory structures of the inner ear do not effectively regenerate, although a latent capacity for regeneration exists at embryonic and perinatal times. We explored the epigenetic basis for this latent regenerative potential in the mouse inner ear and its rapid loss during maturation. In perinatal supporting cells, whose fate is maintained by Notch-mediated lateral inhibition, the hair cell enhancer network is epigenetically primed (H3K4me1) but silenced (active H3K27 de-acetylation and trimethylation). Blocking Notch signaling during the perinatal period of plasticity rapidly eliminates epigenetic silencing and allows supporting cells to transdifferentiate into hair cells. Importantly, H3K4me1 priming of the hair cell enhancers in supporting cells is removed during the first post-natal week, coinciding with the loss of transdifferentiation potential. We hypothesize that enhancer decommissioning during cochlear maturation contributes to the failure of hair cell regeneration in the mature organ of Corti.

| S-EPMC8650127 | biostudies-literature

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