DNA replication initiation factor RECQ4 Q757X IP
Ontology highlight
ABSTRACT:
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
Similar Datasets
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
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
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
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
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
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
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.
2014-03-26 | GSE56171 | GEO
Project description:Transcription shapes DNA replication initiation to preserve genome integrity
| PRJNA731108 | ENA
Project description:The nucleoid occlusion factor Noc controls DNA replication initiation in Staphylococcus aureus
| PRJNA393025 | ENA
Project description:<p><strong>BACKGROUND:</strong> In all living organisms, DNA replication is exquisitely regulated in a wide range of growth conditions to achieve timely and accurate genome duplication prior to cell division. Failures in this regulation cause DNA damage with potentially disastrous consequences for cell viability and human health, including cancer. To cope with these threats, cells tightly control replication initiation using well-known mechanisms. They also couple DNA synthesis to nutrient richness and growth rate through a poorly understood process thought to involve central carbon metabolism. One such process may involve the cross-species conserved pyruvate kinase (PykA) which catalyzes the last reaction of glycolysis. Here we have investigated the role of PykA in regulating DNA replication in the model system <em>Bacillus subtilis.</em></p><p><strong>RESULTS: </strong>On analysing mutants of the catalytic (Cat) and C-terminal (PEPut) domains of <em>B. subtilis</em> PykA we found replication phenotypes in conditions where PykA is dispensable for growth. These phenotypes are independent from the effect of mutations on PykA catalytic activity and are not associated with significant changes in the metabolome. PEPut operates as a nutrient-dependent inhibitor of initiation while Cat acts as a stimulator of replication fork speed. Disruption of either PEPut or Cat replication function dramatically impacted the cell cycle and replication timing even in cells fully proficient in known replication control functions. <em>In vitro</em>, PykA modulates activities of enzymes essential for replication initiation and elongation via functional interactions. Additional experiments showed that PEPut regulates PykA activity and that Cat and PEPut determinants important for PykA catalytic activity regulation are also important for PykA-driven replication functions.</p><p><strong>CONCLUSIONS:</strong> We infer from our findings that PykA typifies a new family of cross-species replication control regulators that drive the metabolic control of replication through a mechanism involving regulatory determinants of PykA catalytic activity. As disruption of PykA replication functions causes dramatic replication defects, we suggest that dysfunctions in this new family of universal replication regulators may pave the path to genetic instability and carcinogenesis.</p>
2022-04-19 | MTBLS4415 | MetaboLights