Quant-seq on COMPASS-degron cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE181708 | GEO | 2023/01/20
REPOSITORIES: GEO
Similar Datasets
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
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,
2023-04-23 | GSE230124 | GEO
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.
2023-04-23 | GSE230123 | GEO
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
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
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
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
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-01-18 | GSE181714 | GEO
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
Project description:TET proteins convert 5-methylcytosine to 5-hydroxymethylcytosine, an emerging dynamic epigenetic state of DNA that can influence transcription. Evidence has linked TET1 function to epigenetic repression complexes, yet mechanistic information, especially for the TET2 and TET3 proteins, remains limited. Here, we show a direct interaction of TET2 and TET3 with O-GlcNAc transferase (OGT). OGT does not appear to influence hmC activity, rather TET2 and TET3 promote OGT activity. TET2/3-OGT co-localize on chromatin at active promoters enriched for H3K4me3 and reduction of either TET2/3 or OGT activity results in a direct decrease in H3K4me3 and concomitant decreased transcription. Further, we show that Host Cell Factor 1 (HCF1), a component of the H3K4 methyltransferase SET1/COMPASS complex, is a specific GlcNAcylation target of TET2/3-OGT, and modification of HCF1 is important for the integrity of SET1/COMPASS. Additionally, we find both TET proteins and OGT activity promote binding of the SET1/COMPASS H3K4 methyltransferase, SETD1A, to chromatin. Finally, studies in Tet2 knockout mouse bone marrow tissue extend and support the data as decreases are observed of global GlcNAcylation and also of H3K4me3, notably at several key regulators of haematopoiesis. Together, our results unveil a step-wise model, involving TET-OGT interactions, promotion of GlcNAcylation, and influence on H3K4me3 via SET1/COMPASS, highlighting a novel means by which TETs may induce transcriptional activation. ChIP-Seq experiments were performed on Illumina HiScanSQ sequencer in wild-type HEK293T cells for H3K4me3 histone marks, O-GlcNAc and HCF1, for HT-TET2, HT-TET3 and HT-OGT in HEK293T cells overexpressing those three fusion proteins and in TET2 Kd HEK293T cells for H3K4me3 histone marks. ChIP-Seqs were also performed in mouse bone marrow tissues for H3K4me3 histone marks, O-GlcNAc, endogenous Tet2 and in Tet2 Ko bone marrow tissues for H3K4me3 histone marks.
2013-02-07 | E-GEOD-36620 | biostudies-arrayexpress