Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Low-level repressive histone marks fine-tune stemness gene transcription in neural stem cells

ABSTRACT: Low-level repressive histone marks fine-tune stemness gene transcription in neural stem cells

PROVIDER: PRJNA902811 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22325600_1.fastq.gz	Fastqsanger.gz
	SRR22325600_2.fastq.gz	Fastqsanger.gz
	SRR22325601_1.fastq.gz	Fastqsanger.gz
	SRR22325601_2.fastq.gz	Fastqsanger.gz
	SRR22325602_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 56

Similar Datasets

Low-level repressive histone marks fine-tune stemness gene transcription in neural stem cells [scRNA-seq]

Project description:Coordinated regulation of stemness gene activity by transcriptional and translational controls poise stem cells for a timely cell-state transition during differentiation. Although important for all stemness-to-differentiation transitions, mechanistic understanding of the fine-tuning of stemness gene transcription is lacking due to the compensatory effect of translational control. We used intermediate neural progenitor (INP) identity commitment to define the mechanisms that fine-tune stemness gene transcription in fly neural stem cells (neuroblasts). We demonstrate that the transcription factor FruitlessC (FruC) binds cis-regulatory elements of most genes uniquely transcribed in neuroblasts. Loss of fruC function alone has no effect on INP commitment but drives INP dedifferentiation when translational control is reduced. FruC negatively regulates gene expression by promoting low-level enrichment of the repressive histone mark H3K27me3 in gene cis-regulatory regions. Identical to fruC loss-of-function, reducing Polycomb Repressive Complex 2 activity increases stemness gene activity. We propose low-level H3K27me3 enrichment fine-tunes stemness gene transcription in stem cells, a mechanism likely conserved from flies to humans.

2023-06-23 | GSE218255 | GEO

Low-level repressive histone marks fine-tune stemness gene transcription in neural stem cells [CUT&Tag]

2023-06-23 | GSE218253 | GEO

Low-level repressive histone marks fine-tune stemness gene transcription in neural stem cells [CUT&Tag]

Project description:Low-level repressive histone marks fine-tune stemness gene transcription in neural stem cells [CUT&Tag]

| PRJNA902809 | ENA

Low-level repressive histone marks fine-tune stemness gene transcription in neural stem cells [scRNA-seq]

Project description:Low-level repressive histone marks fine-tune stemness gene transcription in neural stem cells [scRNA-seq]

| PRJNA902810 | ENA

H3K4me3/H3K27me3 bivalent chromatin function to fine-tune gene expression level

Project description:Bivalency, the paradoxical juxtaposition of transcriptionally activating trimethylation of histone H3 lysine 4 (H3K4me3) and the repressive trimethylation of histone H3 lysine 27 (H3K27me3), has been proposed to decorate developmental genes poised for gene expression regulation. Here, we report development of sequential internally calibrated chromatin immunoprecipitation (Re-ICeChIP-seq), capable of measuring absolute quantities of nucleosomal patterns of histone marks in a genome-wide fashion, combined with in situ control of antibody specificity. Re-ICeChIP-seq of H3K4me3/H3K27me3 in mESC reveals that bivalent genes can be delineated into two classes, distinguished by the nucleosomal ratio of H3K4me3 to H3K27me3. Consistent with the canonical role of bivalency, H3K27me3-rich bivalent nucleosomes demarcate promoters of poorly expressed developmental genes that may be poised for activation or repression. Yet our measurements reveal surprisingly widespread presence of bivalency at promoters of highly-expressed housekeeping genes, characterized by H3K4me3-rich bivalent nucleosomes. Moreover, the ratio of H3K4me3 to H3K27me3 at transcription start sites better correlates with gene expression than H3K4me3 or H3K27me3 alone, suggesting cooperation between opposing marks to fine-tune gene expression. Finally, we report that major H3K4 methyltransferases exhibit wide acceptance of various H3K27me3 substrates.

2021-01-04 | GSE108747 | GEO

Low-level repressive histone marks fine-tune stemness gene transcription in neural stem cells

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

2023-06-22 | GSE218257 | GEO

Independence of Repressive Histone Marks and Chromatin Compaction during Senescent Heterochromatic Layer Formation

Project description:The expansion of repressive epigenetic marks has been implicated in heterochromatin formation during embryonic development, but the general applicability of this mechanism is unclear. Here we show that nuclear rearrangement of repressive histone marks H3K9me3 and H3K27me3 into non-overlapping structural layers characterizes senescence-associated heterochromatic foci (SAHF) formation in human fibroblasts. However, the global landscape of these repressive marks remains unchanged upon SAHF formation, suggesting that in somatic cells heterochromatin can be formed through the spatial repositioning of pre-existing repressively marked histones. This model is reinforced by the correlation of pre-senescent replication timing with both the subsequent layered structure of SAHFs and the global landscape of the repressive marks, allowing us to integrate microscopic and genomic information. Furthermore, modulation of SAHF structure does not affect the occupancy of these repressive marks nor vice versa. These experiments reveal that high-order heterochromatin formation and epigenetic remodeling of the genome can be discrete events. Profile comparison of normal growing (control) and Ras-induced senescent IMR90 cells.

2012-06-30 | E-GEOD-38460 | biostudies-arrayexpress

Independence of Repressive Histone Marks and Chromatin Compaction during Senescent Heterochromatic Layer Formation

Project description:This SuperSeries is composed of the following subset Series: GSE38410: Independence of Repressive Histone Marks and Chromatin Compaction during Senescent Heterochromatic Layer Formation (mRNA) GSE38442: Independence of Repressive Histone Marks and Chromatin Compaction during Senescent Heterochromatic Layer Formation (ChIP-Seq) Refer to individual Series

2012-07-08 | E-GEOD-38448 | biostudies-arrayexpress

H3K4me3/H3K27me3 bivalent chromatin function to fine-tune gene expression level

Project description:H3K4me3/H3K27me3 bivalent chromatin function to fine-tune gene expression level

| PRJNA428482 | ENA

Independence of Repressive Histone Marks and Chromatin Compaction during Senescent Heterochromatic Layer Formation (mRNA)

Project description:The expansion of repressive epigenetic marks has been implicated in heterochromatin formation during embryonic development, but the general applicability of this mechanism is unclear. Here we show that nuclear rearrangement of repressive histone marks H3K9me3 and H3K27me3 into non-overlapping structural layers characterizes senescence-associated heterochromatic foci (SAHF) formation in human fibroblasts. However, the global landscape of these repressive marks remains unchanged upon SAHF formation, suggesting that in somatic cells heterochromatin can be formed through the spatial repositioning of pre-existing repressively marked histones. This model is reinforced by the correlation of pre-senescent replication timing with both the subsequent layered structure of SAHFs and the global landscape of the repressive marks, allowing us to integrate microscopic and genomic information. Furthermore, modulation of SAHF structure does not affect the occupancy of these repressive marks nor vice versa. These experiments reveal that high-order heterochromatin formation and epigenetic remodeling of the genome can be discrete events. mRNA expression profiles were compared between normal growing (control) and Ras-induced senescent IMR90 cells. Each includes 5 biological replicates.

2012-07-08 | E-GEOD-38410 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data