Genome-wide map of BrdU incorporation and sororin binding in HeLa cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB12214 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1194870.fastq.gz | Fastqsanger.gz | |||
| ERR1194880.fastq.gz | Fastqsanger.gz | |||
| ERR1194871.fastq.gz | Fastqsanger.gz | |||
| ERR1194881.fastq.gz | Fastqsanger.gz | |||
| ERR1194872.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 19 |
Similar Datasets
Project description:Differential acetylation of SMC3 relative to BrdU as a function of ESCO2 motif PBMA deletion and depletion of ESCO1
2017-10-17 | GSE105004 | GEO
Project description:Genome-wide map of BrdU incorporation, SMC3 and SMC3(ac) binding in HeLa cells in early S phase
| PRJNA414403 | ENA
Project description:Drosophila and mammalian hematopoiesis share several similarities that ranges from phases to the battery of transcription factors and signaling molecules that execute this process. These resounding similarities along with the rich genetic tools available in fruitfly makes it a popular invertebrate model to study blood cell development both during normal and aberrant conditions. The larval system is the most extensively studied to date. Several studies have shown that these hemocytes just like mammalian counterpart proliferate and get routinely regenerated upon infection. However, employing the same protocol it was concluded that blood cell proliferation although abundant in larval stages is absent in adult fruitfly. The current protocol describes the strategies that can be employed to document the hemocyte proliferation in adulthood. The fact that a subset of blood cells tucked away in the hematopoietic hub are not locked in senescence, rather they still harbour the proliferative capacity to tide over challenges was successfully demonstrated by this method. Although we have adopted bacterial infection as a bait to evoke this proliferative capacity of the hemocytes, we envision that it can also efficiently characterize the proliferative responses of hemocytes in tumorigenic conditions as well as scenarios of environmental and metabolic stresses during adulthood.
| S-EPMC5989151 | biostudies-literature
Project description:RNA transcription and DNA replication both use DNA as a substrate, that however can be engaged only by one of them at any given time. Consequently, conflicts between transcription and replication significantly affect genome stability and human health. To understand the reciprocal interplay between transcription and replication in human cells, we performed a genome-wide analysis of the two processes throughout S-phase. We found that transcription persists during replication, with direct consequences for replication progression through genes and sites of DNA damage. Importantly however, we also found that transcription start sites will not be replicated together with the surrounding regions, and remain under-replicated throughout S-phase. DNA synthesis across transcription start sites occurs specifically when cells enter mitosis, because the RNA Polymerase II is removed at that point from the majority of the genes. Intriguingly, this G2/M DNA synthesis is not associated with increased DNA damage and occurs at very high frequency.
2021-02-17 | GSE136288 | GEO
Project description:RNA transcription and DNA replication both use DNA as a substrate, that however can be engaged only by one of them at any given time. Consequently, conflicts between transcription and replication significantly affect genome stability and human health. To understand the reciprocal interplay between transcription and replication in human cells, we performed a genome-wide analysis of the two processes throughout S-phase. We found that transcription persists during replication, with direct consequences for replication progression through genes and sites of DNA damage. Importantly however, we also found that transcription start sites will not be replicated together with the surrounding regions, and remain under-replicated throughout S-phase. DNA synthesis across transcription start sites occurs specifically when cells enter mitosis, because the RNA Polymerase II is removed at that point from the majority of the genes. Intriguingly, this G2/M DNA synthesis is not associated with increased DNA damage and occurs at very high frequency.
2021-02-17 | GSE136293 | GEO
Project description:BackgroundThymidine analogs have long been recognized for their ability to randomly incorporate into DNA. However, the precise mechanisms through which thymidine analogs facilitate cell fate transition remains unclear.ResultsHere, we discovered a strong correlation between the dosage dependence of thymidine analogs and their ability to overcome reprogramming barrier. The extraembryonic endoderm (XEN) state seems to be a cell's selective response to DNA damage repair (DDR), offering a shortcut to overcome reprogramming barriers. Meanwhile, we found that homologous recombination repair (HRR) pathway causes an overall epigenetic reshaping of cells and enabling them to overcome greater barriers. This response leads to the creation of a hypomethylated environment, which facilitates the transition of cell fate in various reprogramming systems. We term this mechanism as Epigenetic Reshaping through Damage (ERD).ConclusionOverall, our study finds that BrdU/IdU can activate the DNA damage repair pathway (HRR), leading to increased histone acetylation and genome-wide DNA demethylation, regulating somatic cell reprogramming. This offers valuable insights into mechanisms underlying cell fate transition.
| S-EPMC10792782 | biostudies-literature
Project description:RNA transcription and DNA replication both use DNA as a substrate, that however can be engaged only by one of them at any given time. Consequently, conflicts between transcription and replication significantly affect genome stability and human health. To understand the reciprocal interplay between transcription and replication in human cells, we performed a genome-wide analysis of the two processes throughout S-phase. We found that transcription persists during replication, with direct consequences for replication progression through genes and sites of DNA damage. Importantly however, we also found that transcription start sites will not be replicated together with the surrounding regions, and remain under-replicated throughout S-phase. DNA synthesis across transcription start sites occurs specifically when cells enter mitosis, because the RNA Polymerase II is removed at that point from the majority of the genes. Intriguingly, this G2/M DNA synthesis is not associated with increased DNA damage and occurs at very high frequency.
2021-02-17 | GSE160842 | GEO
Project description:The interchromatin space in the cell nucleus contains various membrane-less nuclear bodies. Recent findings indicate that nuclear speckles, comprising a distinct nuclear body, exhibit interactions with certain chromatin regions in a ground state. Key questions are how this ground state of chromatin-nuclear speckle association is established and what are the gene regulatory roles of this layer of nuclear organization. We report here that chromatin structural factors CTCF and cohesin are required for full ground state association between DNA and nuclear speckles. Disruption of ground state DNA-speckle contacts via either CTCF depletion or cohesin depletion had minor effects on basal level expression of speckle-associated genes, however we show strong negative effects on stimulus-dependent induction of speckle-associated genes. We identified a putative speckle targeting motif (STM) within cohesin subunit RAD21 and demonstrated that the STM is required for chromatin-nuclear speckle association. In contrast to reduction of CTCF or RAD21, depletion of the cohesin releasing factor WAPL stabilized cohesin on chromatin and DNA-speckle contacts, resulting in enhanced inducibility of speckle-associated genes. In addition, we observed disruption of chromatin-nuclear speckle association in patient derived cells with Cornelia de Lange syndrome (CdLS), a congenital neurodevelopmental diagnosis involving defective cohesin pathways, thus revealing nuclear speckles as an avenue for therapeutic inquiry. In summary, our findings reveal a mechanism to establish the ground organizational state of chromatin-speckle association, to promote gene inducibility, and with relevance to human disease.
2024-11-08 | GSE273618 | GEO
Project description:Cohesin acetylation by Eco1 during DNA replication establishes sister chromatid cohesion. We show that acetylation makes cohesin resistant to Wapl activity from S-phase until mitosis. Wapl turns out to be a key regulator of cohesin dynamics on chromosomes by controling cohesin maintenance following its establishment in S-phase and its role in chromosome condensation. The Affymetrix Saccharomyces cerevisiae Chip Tiling 1.0F Arrays were used to analyze the incorporation of BrdU in Saccharomyces cerevisiae in S-phase arrested cells.
2012-11-22 | E-GEOD-42456 | biostudies-arrayexpress
Project description:Cohesin participates in loop formation by extruding DNA fibers from its ring-shaped structure. Cohesin dysfunction eliminates chromatin loops but only causes modest transcription perturbation, which cannot fully explain the frequently observed mutations of cohesin in various cancers. Here, we found that DNA replication initiates at more than one thousand extra dormant origins after acute depletion of RAD21, a core subunit of cohesin, resulting in earlier replicating timing at approximately 30% of the human genomic regions. In contrast, CTCF is dispensable for suppressing the early firing of dormant origins that are distributed away from the loop boundaries. Furthermore, greatly elevated levels of gross DNA breaks and genome-wide chromosomal translocations arise in RAD21-depleted cells, accompanied by dysregulated replication timing at dozens of hotspot genes. Thus, we conclude that cohesin coordinates DNA replication initiation to ensure proper replication timing and safeguards genome integrity.
2022-07-31 | GSE189760 | GEO