Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DNA replication initiation factor RECQ4 Q757X IP

ABSTRACT: DNA replication initiation factor RECQ4 Q757X IP from HEK293 cells

INSTRUMENT(S): Orbitrap Eclipse

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Yilun Liu

PROVIDER: MSV000088653 | MassIVE | Thu Jan 06 14:23:00 GMT 2022

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gidvani2012 - DNA replication initiation model in S. Cevevisiae

Project description:A quantitative model of the initiation of DNA replication in Saccharomyces cerevisiae predicts the effects of system perturbations. Model is encoded by Matthew Maire and submitted in BioModels by Krishna Kumar Tiwari.

2020-05-06 | MODEL2003180001 | BioModels

HDACs act on ribosomal DNA to control the yeast replication program and the competition between origins for limiting initiation factors [ChIP-seq]

Project description:In S. cerevisiae, replication timing is controlled by epigenetic mechanisms restricting the accessibility of origins to limiting initiation factors. About 30% of these origins are located within repetitive DNA sequences such as the ribosomal DNA (rDNA) array, but their regulation is poorly understood. Here, we have investigated how histone deacetylases (HDACs) control the replication program in budding yeast. This analysis revealed that two HDACs, Rpd3 and Sir2, control replication timing in an opposite manner. Whereas Rpd3 delays initiation at late origins, Sir2 is required for the timely activation of early origins. Moreover, Sir2 represses initiation at rDNA origins whereas Rpd3 counteracts this effect. Remarkably, deletion of SIR2 restored normal replication in rpd3 cells by reactivating rDNA origins. Together, these data indicate that HDACs control the replication timing program in budding yeast by modulating the ability of repeated origins to compete with single-copy origins for limiting initiation factors. BrdU-IP-seq analysis of origin activity in wt, sir2 and rpd3 cells, aligned against genomic DNA (sacCer3) and rDNA sequences Please note that the wt WCE #1 and #2 samples are whole-cell extracts from wild-type cells arrested in HU that were used to calculate the log ratio of the BrdU IP #1 and #2 batches, respectively.

2014-05-14 | E-GEOD-57617 | biostudies-arrayexpress

HDACs act on ribosomal DNA to control the yeast replication program and the competition between origins for limiting initiation factors

Project description:In S. cerevisiae, replication timing is controlled by epigenetic mechanisms restricting the accessibility of origins to limiting initiation factors. About 30% of these origins are located within repetitive DNA sequences such as the ribosomal DNA (rDNA) array, but their regulation is poorly understood. Here, we have investigated how histone deacetylases (HDACs) control the replication program in budding yeast. This analysis revealed that two HDACs, Rpd3 and Sir2, control replication timing in an opposite manner. Whereas Rpd3 delays initiation at late origins, Sir2 is required for the timely activation of early origins. Moreover, Sir2 represses initiation at rDNA origins whereas Rpd3 counteracts this effect. Remarkably, deletion of SIR2 restored normal replication in rpd3 cells by reactivating rDNA origins. Together, these data indicate that HDACs control the replication timing program in budding yeast by modulating the ability of repeated origins to compete with single-copy origins for limiting initiation factors. BrdU-IP-chip analysis of origin usage in different yeast HDAC mutants

2014-03-26 | E-GEOD-56171 | biostudies-arrayexpress

Loss of Ezh2 function reshapes DNA replication initiation landscape

Project description:DNA replication initiation is made possible by the assembly of pre- replication complexes (Pre-RCs) at genomic locations called DNA replication initiation sites (origins) during G1-phase. Although there are no conserved characteristics of metazoan origins on which Pre-RCs form, previous findings suggest that origins are strongly associated with open, active chromatin regions of the genome such as promoters, enhancers, and active histone marks. However, over a third of transcriptionally silent genes associate with DNA replication initiation activity in mESC cells, and most of these genes are bound and repressed by the Polycomb repressive complex 2 (PRC2) through the repressive H3K27me3 mark. This is the strongest observed association of an epigenetic regulator element with replication origin activity. Thus, I wished to ask whether Polycomb-mediated gene repression plays a direct role in the recruitment of DNA replication origins activity to silent genes. I comprehensively characterized the consequences of PRC2 catalytic activity (EZH2 subunit) depletion on the activity of DNA replication origins in mESC through a genome-wide evaluation. My findings suggest that absence of EZH2 results in increased DNA replication initiation activity at EZH2-bound sites. Interestingly, the increase in DNA replication initiation activity does not correlate with transcriptional de-repression or acquisition of the activating marks H3K4me3 and H3K27ac but loss of the repressive H3K27me3 mark leading to increased accessibility of chromatin.

2023-04-19 | GSE205756 | GEO

DNA replication initiation RECQ4 WT

Project description:FLAG-RECQ4 IP Mass spec from HEK293 cells depleted with the endogenous RECQ4 gene. peak file 77274.mzXML. Result file 77274.mzid

2022-01-06 | MSV000088652 | MassIVE

Transcription shapes DNA replication initiation to preserve genome integrity

Project description:We develop a high-throughput nucleoside analog incorporation sequencing assay and identify thousands of early replication initiation zones (ERIZs) in both mouse and human cells. The identified ERIZs fall in open chromatin compartments while are mutually exclusive with transcription elongation and occupy mainly non-transcribed regions adjacent to transcribed regions. Furthermore, we reveal that RNA polymerase II actively redistributes the chromatin-encircled mini-chromosome maintenance (MCM) complex but not the origin-recognition complex (ORC) to actively restrict early DNA replication initiation outside of transcribed regions. The coupling of RNA polymerase II and MCM is further validated by detected MCM accumulation and DNA replication initiation after RNA polymerase II stalling via anchoring nuclease-dead Cas9 at the transcribed genes. Importantly, we also find that the orchestration of DNA replication initiation by transcription can efficiently prevent gross DNA damage.

2021-05-20 | GSE174680 | GEO

HDACs act on ribosomal DNA to control the yeast replication program and the competition between origins for limiting initiation factors [BrdU-IP-chip]

2014-03-26 | GSE56171 | GEO

Transcription shapes DNA replication initiation to preserve genome integrity

Project description:Transcription shapes DNA replication initiation to preserve genome integrity

| PRJNA731108 | ENA

Loss of Ezh2 function reshapes DNA replication initiation landscape

Project description:Loss of Ezh2 function reshapes DNA replication initiation landscape

| PRJNA847445 | ENA

The nucleoid occlusion factor Noc controls DNA replication initiation in Staphylococcus aureus

Project description:The nucleoid occlusion factor Noc controls DNA replication initiation in Staphylococcus aureus

| PRJNA393025 | ENA