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Topoisomerase 1 activity during mitotic transcription favors the transition from mitosis to G1 [SLAM-seq]

ABSTRACT: Topoisomerase 1 activity during mitotic transcription favors the transition from mitosis to G1 [SLAM-seq]

PROVIDER: PRJNA718531 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14107563.fastq.gz	Fastqsanger.gz
	SRR14107564.fastq.gz	Fastqsanger.gz
	SRR14107565.fastq.gz	Fastqsanger.gz
	SRR14107566.fastq.gz	Fastqsanger.gz
	SRR14107567.fastq.gz	Fastqsanger.gz

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Similar Datasets

Topoisomerase 1 activity during mitotic transcription favors the transition from mitosis to G1

Project description:Topoisomerase 1 activity during mitotic transcription favors the transition from mitosis to G1

| PRJNA718529 | ENA

Topoisomerase 1 activity during mitotic transcription favors the transition from mitosis to G1 [ChIP-seq]

Project description:Topoisomerase 1 activity during mitotic transcription favors the transition from mitosis to G1 [ChIP-seq]

| PRJNA718530 | ENA

Topoisomerase 1 activity during mitotic transcription favors the transition from mitosis to G1 [SLAM-seq]

Project description:Using SLAM-seq to capture de novo synthesized polyadenylated RNAs, we quantitated changes in nascent RNA expression, as well as in total RNA expression.

2021-11-11 | GSE171133 | GEO

Topoisomerase 1 activity during mitotic transcription favors the transition from mitosis to G1 [ChIP-seq]

Project description:By following chromatin occupancy of RNAPII and TOP1 using ChIP-seq throughout mitosis, we found that TOP1 is required for RNAPII translocation along genes. The stimulation of TOP1 activity through its interaction with RNAPII during elongation, allowed RNAPII clearance from genes in prometaphase and enabled proper chromosomal segregation. Interference with the TOP1-RNAPII interaction or acute depletion of TOP1 at the onset of mitosis impaired RNAPII spiking at promoters, which is necessary for the first pioneering round of transcription during mitotic exit, and triggered defects in the transcriptional program of the post-mitotic cells.

2021-11-11 | GSE171132 | GEO

Mitotic chromosomes are self-entangled and disentangle through a Topoisomerase II-dependent two stage exit from mitosis

Project description:The topological state of chromosomes determines their mechanical properties, dynamics, and function. Recent work indicated that interphase chromosomes are largely free of entanglements. Here, we use Hi-C, polymer simulations and multi-contact 3C, and propose that, in contrast, mitotic chromosomes are self-entangled. We explore how a mitotic self-entangled state is converted into an unentangled interphase state during mitotic exit. Most mitotic entanglements are removed during anaphase/telophase, with remaining ones removed during early G1, in a Topoisomerase II-dependent process. Polymer models suggest a two-stage disentanglement pathway: first, decondensation of mitotic chromosomes with remaining condensin loops produces entropic forces that bias Topoisomerase II activity towards decatenation. At the second stage, the loops are released, and formation of new entanglements is prevented by lower Topoisomerase II activity, allowing the establishment of unentangled and territorial G1 chromosomes. When mitotic entanglements are not removed, in experiment and models, a normal interphase state cannot be acquired.

2024-03-07 | GSE198610 | GEO

Topoisomerase 1 activity during mitotic transcription favors the transition from mitosis to G1

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

2021-11-11 | GSE171134 | GEO

Mitotic Transcription and Waves of Gene Reactivation During Mitotic Exit

Project description:The genome is thought to be transcriptionally silent during mitosis. Technical limitations have prevented the sensitive mapping of mitotic transcription and transcription reactivation during mitotic exit, and thus the networks by which transcriptome dynamics govern the generation of daughter cells have been unclear. We used 5-ethynyluridine to pulse-label intact transcripts during mitosis and mitotic exit and find that the first round of transcription activates genes that are involved in macromolecular synthesis, rather than cell identity. Many interphase genes exhibit residual transcription in mitosis, as confirmed by different methods of assessment, and a subset of genes are more highly transcribed in mitosis than in interphase. We suggest that mitotic transcription may serve an epigenetic function in restoring proper transcription patterns during mitotic exit.

2017-09-20 | GSE87476 | GEO

TDP1 phosphorylation at S61 promotes Top1cc repair via the MUS81-dependent pathway during mitosis

Project description:Topoisomerase 1 (Top1) removes supercoils from DNA during replication and transcription, is critical for mitotic progression to the G1 phase, and ensures DNA topology. Tyrosyl-DNA phosphodiesterase 1 (TDP1) mediates the removal of trapped Top1-DNA covalent complexes (Top1ccs). Here, we identify CDK1-dependent phosphorylation of TDP1 at S61 residue during mitosis. TDP1 defective for S61 phosphorylation (TDP1S61A) is trapped on the mitotic chromosomes, triggering DNA damage and mitotic defects. Moreover, we show that Top1cc repair in mitosis occurs via MUS81-dependent mitotic DNA repair mechanism. Replication stress (RS) induced by Camptothecin (CPT) or Aphidicolin (APH) leads to TDP1S61A enrichment at common fragile sites (CFSs), which over-stimulates MUS81-dependent chromatid breaks, anaphase bridges, and micronuclei, ultimately culminating in 53BP1 nuclear bodies in the G1-phase. Our findings provide a new insight into the cell cycle-dependent regulation of TDP1 dynamics forthe repair of trapped Top1ccs during mitosis that prevents genomic instability following RS.

2024-06-26 | PXD053309 | Pride

Loss of H3K9 tri-methylation alters mitotic chromosome compaction and transcription factor retention during mitosis

Project description:Recent studies have shown that repressive chromatin machinery, including DNA methyltransferases (DNMTs) and Polycomb Repressor Complexes (PRCs), bind to chromosomes throughout mitosis and their depletion results in increased chromosome size. Enzymes that catalyse H3K9 methylation, such as Suv39h1, Suv39h2, G9a, GLP are also retained by mitotic chromosomes. Surprisingly however, mutants lacking H3K9me3 have unusually small and compact mitotic chromosomes that are associated with increased H3S10ph and H3K27me3 levels. Despite these differences, chromatin accessibility, as measured by ATAC-seq, was broadly similar between genotypes. Chromosome size and centromere compaction in these mutants was rescued by providing exogenous Suv39h1, or inhibiting Ezh2 activity. Quantitative proteomic comparisons of native mitotic chromosomes isolated from wildtype versus Suv39h1,2 double null ESCs revealed that H3K9me3 was essential for the efficient retention of bookmarking factors such as Esrrb. These results highlight an unexpected role for repressive heterochromatin domains in preserving transcription factor binding through mitosis, and underscore the importance of H3K9me3 for sustaining chromosome architecture and epigenetic memory during cell division.

2023-01-17 | GSE195767 | GEO

Topoisomerase I (TOP1) is a functional mitotic interactor of the bookmarking factor HNF1B [RNAseq_786O]

Project description:HNF1B (Hepatocyte Nuclear Factor 1-Beta) is a POU-homeobox transcription factor expressed in kidney and frequently mutated in patients suffering from Congenital Anomalies of the Kidney and the Urinary Tract (CAKUT). HNF1B is a bookmarking factor, able to bind mitotic chromatin and necessary for the post-mitotic reactivation of gene expression. In order to characterize the molecular functions of HNF1B as a bookmarking factor, we performed ChIPseq on asynchronous and mitotic renal cells. We developed a novel ChIP method with a non-aqueous crosslinking (NAQC) to circumvent the well-known artefactual effects of formaldehyde crosslinking of mitotic chromosomes. NAQC-ChIP allowed the retention of the mitotic signal that was lost with a regular ChIP. With this novel methodology, we show that the vast majority HNF1B binding sites detected in asynchronous cells are also bound in mitosis.

2024-10-01 | GSE245071 | GEO

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