Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Quant-seq on COMPASS-degron cells

ABSTRACT: Here, we showed that acute lost H3K4me3 induces rapid reduction in global transcription with progressively increase in magnitude over the time-course cooccurrence with lost all H3K4 methylations,

ORGANISM(S): Mus musculus

PROVIDER: GSE181708 | GEO | 2023/01/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ChIP-seq on COMPASS-degron cells

Project description:Here, we showed that acute lost H3K4me3 induces rapid reduction in global transcription with progressively increase in magnitude over the time-course cooccurrence with lost all H3K4 methylations. To further determine the effects of COMPASS subunits degradation on H3K4 methylations occupancies genome-wide, we performed time-course spike-in chromatin immunoprecipitation and sequencing (ChIP-seq, also known as ChIP-Rx) analysis in both degron systems.

2023-01-20 | GSE181892 | GEO

SLAM-seq on INTS11-degron cells

2023-04-23 | GSE230124 | GEO

ChIP-seq on INTS11-degron cells

2023-04-23 | GSE230123 | GEO

Quant-seq on COMPASS-degron cells

Project description:Quant-seq on COMPASS-degron cells

| PRJNA753077 | ENA

TT-seq on COMPASS-degron cells

Project description:Here, we use elongation velocity analysis showed that acute loss H3K4me3 caused a general transcriptome-wide attenuation of elongation velocity in cells.

2023-01-20 | GSE181712 | GEO

The Set1 N-terminal domain and Swd2 interact with the RNA polymerase II CTD to recruit COMPASS

Project description:Methylation of histone H3 lysine 4 (H3K4) by the Set1/COMPASS complex is coupled with active transcription, and this modification is important for regulating gene expression. Set1/COMPASS associates with the RNA polymerase II (RNApII) C-terminal domain (CTD) to establish proper levels and distribution of H3K4 methylations.To ask how the Set1-RNApII CTD binding affects the occupancy and overall level of H3K4 methylations, ChIP-Seq was pefromed in cells transformed with full length or N-terminal truncated Set1. Our results indicate that Set1-RNApII CTD interaction is necessary for maintaining H3K4 methylations throughout the genes.

2019-10-02 | GSE138281 | GEO

mNET-seq on COMPASS-degron cells

Project description:We measured the the dwell time of existed paused RNAPII at the promoter by mammalian native elongating transcript sequencing (mNET-seq). We found a median RNAPII half-life of 5.3 min at protein-coding genes in DMSO pre-treated control mESCs, whereas the RNAPII half-life at these genes significantly slowdown to 8.96 min when pre-treated with Auxin in the DPY30-mAID degron cell. The data suggested that loss H3K4me3 directly slows down the release of paused RNAPII throughout genes.

2023-01-20 | GSE181686 | GEO

Context Dependency of Set1/COMPASS Mediated H3 Lysine 4 Trimethylation

Project description:The stimulation of trimethylation of histone H3 lysine 4 (H3K4) by H2B monoubiquitination (H2Bub) has been widely studied with multiple mechanisms proposed for this form of histone crosstalk. Cps35/Swd2 within COMPASS is considered to bridge these processes. However, a truncated form of Set1 (762-Set1) is reported to function in H3K4 trimethylation without interacting with Cps35/Swd2, and such crosstalk is attributed to the n-SET domain of Set1 and its interaction with the Cps40/Spp1 subunit of COMPASS. Here, we use biochemical, structural, in vivo, and ChIP-seq approaches to demonstrate that Cps40/Spp1 and the n-SET domain of Set1 are required for the stability of Set1 and not the crosstalk. Furthermore, the apparent wild-type levels of H3K4 trimethylation (H3K4me3) in the 762-Set1 strain is due to rogue methylase activity of this mutant resulting in the mislocalization of H3K4me3 from the promoter-proximal regions to gene bodies and intergenic regions. We have also performed detailed screens and identified yeast strains lacking H2Bub, but containing intact H2Bub enzymes, that have normal levels of H3K4me3, suggesting that ubiquitination may not directly stimulate COMPASS, but rather works in a context of the PAF and Rad6/Bre1 complexes. Our study demonstrates that the ubiquitination machinery and Cps35/Swd2 function to focus COMPASS’ H3K4me3 activity at promoter-proximal regions in a context dependent manner. ChIP-Seq for H3K4ME3 in S. cerevisie wild-type strains and strains expressing a truncated form of Set1: aa762-1080 Set1. H3K4ME3 ChIP-Seq was also compared for wild-type, leo1 knockout, and chd1 knockout strains

2014-01-09 | E-GEOD-53241 | biostudies-arrayexpress

COMPASS-degron cells

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

2023-01-18 | GSE181714 | GEO

H3K4me3 recognition by the COMPASS complex guides de novo histone methylation to restore the symmetric distribution of H3K4me3 following DNA replication

Project description:During DNA replication, histones in nucleosomes ahead of DNA replication forks are evicted and then distributed equally onto leading and lagging strands. Mcm2, a subunit of the replicative MCM helicase, participates in the transfer of parental H3-H4 marked by H3K4me3 to lagging strands. Mutations in Mcm2 (Mcm2-3A) result in enrichment of H3K4me3 at leading strands following DNA replication. Here, we show that mcm2-3A mutant cells partially recover the H3K4me3 lost at lagging strands, with a faster recovery at highly transcribed genes than lowly ones, before mitosis. Furthermore, the H3K4 methyltransferase complex COMPASS is essential in the recovery of H3K4me3, irrespective of transcription status. Finally, H3K4me3 recognition (read) by COMPASS is also important for the restoration (write) of this mark. We suggest that both gene transcription and the “read and write” mechanism contribute to the restoration of H3K4me3, with the later mechanism more important for lowly transcribed chromatin.

2022-04-13 | GSE184188 | GEO

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