Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A Top2 and Hmo1-mediated genome architectural pathway preventing chromosome fragility.

ABSTRACT: Specialized topoisomerases solve the topological constraints arising when replication forks encounter transcription. We have investigated Top2 contribution in S phase transcription. Specifically in S phase, Top2 binds intergenic regions close to transcribed genes without influencing their transcription. The Top2-bound loci exhibit low nucleosome density and accumulate yH2A when Top2 is defective. These intergenic loci associate with the HMG-protein Hmo1 throughout the cell cycle and are refractory to the histone variant Htz1. In top2 mutants, Hmo1 is deleterious and accumulates at pericentromeric regions in G2/M. Our data indicate that Top2 is dispensable for transcription and that Hmo1 and Top2 bind in the proximity of genes transcribed in S phase suppressing chromosome fragility at the M-G1 transition. We propose that an Hmo1-dependent epigenetic signature together with Top2 mediate a S-phasen architectural pathway controlling replicon dynamics when forks encounter transcriptionto preserve genome integrity. Signal tracks in BED format suitable for visualization on the UCSC genome browser can be found at http://bio.ifom-ieo-campus.it/supplementary/Bermejo_et_al_CELL_2009

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE16258 | GEO | 2009/09/05

SECONDARY ACCESSION(S): PRJNA115093

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Effect of top2 and hmo1 on chromatin architecture and transcription in yeast

Project description:DNA topoisomerase-2 and high mobility group protein Hmo1 are known to regulate chromatin architecture by regulating gene boundaries. Here we report how these proteins affect global RNA level after inactivation of Top2 and Hmo1. Our data indicate that inactivating Hmo1 has a drastic effect on transcription levels of 20% yeast genes, however, this phenomenon can slightly be rescued by inactivating Top2 functions. Also, we study the Top2 and Top1 role in nucleosome architecture with and without expressing E.coli TopA. In top2-1;top1∆ condition with TopA expressed, it affects the nucleosome occupancy at the global level compared with top2-1;top1∆-Control plasmid. The ChIA-PET (Chromatin interaction analysis by paired-end tag sequencing) method is used to address whether a specific protein is engaged in the chromosomal interactions. Epitope tagged Top2 protein is used as probe in ChIA-PET experiments to map Top2 mediated chromatin-chromatin interactions.

2018-07-02 | GSE114444 | GEO

Sen1 and Rrm3 ensure permissive topological conditions for replication termination [ChIP-seq]

Project description:Replication forks terminate at TERs and telomeres. Forks that converge or encounter transcription generate topological stress. Combining genetic, genomic and imaging approaches we found that Rrm3hPif1 and Sen1hSenataxin helicases assist termination at TERs, Sen1 at telomeres. rrm3 and sen1 are synthetic lethal, fail to terminate replication exhibiting lagging chromosomes and fragility at TERs and telomeres. sen1 rrm3 build up RNA-DNA hybrids at TERs, sen1 accumulates RNPII at TERs and telomeres. Double mutants exhibit X-shaped gapped or reversed converging forks. Rrm3 and Sen1 restrain Top1 and Top2 activities, preventing toxic accumulation of positive supercoil at TERs and telomeres. We suggest that Rrm3 and Sen1 coordinate the activities of fork-associated Top1 and Top2 with those of gene loop-associated Top1 and Top2 by preventing DNA and RNA polymerases slowing down when forks encounter transcription head-on or codirectionally, respectively. Hence Rrm3 and Sen1 are essential to generate permissive topological conditions for replication termination.

2022-10-11 | GSE214925 | GEO

Sen1 and Rrm3 ensure permissive topological conditions for replication termination [ChIP-chip]

2022-10-11 | GSE214908 | GEO

Hmo1 ChIP-chip

Project description:Yeast Hmo1 ChIP-chip in triplicate with single untagged control Yeast Hmo1 ChIP-chip was performed in yDH419 (Hmo1-3myc) in triplicate using anti-myc (9E10 monoclonal antibody). A control experiment was performed using the untagged isogenic strain, BY4742

2010-07-01 | E-GEOD-4046 | biostudies-arrayexpress

Effect of top2 and hmo1 on chromatin architecture and transcription in yeast

Project description:Effect of top2 and hmo1 on chromatin architecture and transcription in yeast

| PRJNA471353 | ENA

Top1 and Top2-mediated replication fork integrity

Project description:DNA topoisomerases solve topological problems during chromosome metabolism. We investigated where and when Top1 and Top2 are recruited on replicating chromosomes and how their inactivation affects fork integrity and DNA damage checkpoint activation. We show that, in the context of replicating chromatin, Top1 and Top2 act within a 600 bp region spanning the moving forks. Top2 exhibits additional S-phase clusters at specific intergenic loci, mostly containing promoters. TOP1 ablation does not affect fork progression and stability and does not cause activation of the Rad53 checkpoint kinase. top2 mutants accumulate sister chromatid junctions in S phase without affecting fork progression and activate Rad53 at the M/G1 transition. top1 top2 double mutants exhibit fork block and processing, and phosphorylation of Rad53 and γH2A in S phase. The exonuclease Exo1 influences fork processing and DNA damage checkpoint activation in top1 top2 mutants. Our data are consistent with a coordinated action of Top1 and Top2 in counteracting the accumulation of torsional stress and sister chromatid entanglement at replication forks, thus preventing the diffusion of topological changes along large chromosomal regions. A failure in resolving fork-related topological constrains during S phase may therefore result in abnormal chromosome transitions, DNA damage checkpoint activation and chromosome breakage during segregation. Keywords: ChIP-chip analysis

2007-08-01 | GSE8305 | GEO

Investigating the role of Hmo1 in transcription by Pol I in yeast.

Project description:The purpose of this study was to investigate the role of the yeast protein, high mobility group protein (Hmo1), in rRNA synthesis. For over twenty years, Hmo1 has been proposed to be an activator of transcription by Pol I, but its regulatory mechanism remains largely undefined. Therefore, we used native elongating transcript sequencing (NET-seq) to explore the role of this factor in transcription by Pol I. Our NET-seq results demonstrated that in cells lacking Hmo1 (hmo1D), Pol I occupancy was significantly increased across the rDNA template, indicating an increased pause propensity in these cells. These data suggest that Hmo1 is an important transcription elongation factor for Pol I.

2023-11-20 | GSE247981 | GEO

Hmo1 ChIP-chip

Project description:Yeast Hmo1 ChIP-chip in triplicate with single untagged control Keywords: ChIP-chip

2006-01-19 | GSE4046 | GEO

Dormant origins and fork protection mechanisms rescue sister forks arrested by transcription

Project description:Yeast Sen1Senataxin is a RNA/DNA helicase that preserves replication forks across RNA Polymerase II-transcribed genes by counteracting RNA:DNA hybrids accumulation. We show that in Sen1-depleted cells early forks clashing head-on with transcription halt, and impair progression of sister forks within the same replicon. Unsolved replication-transcription collisions trigger the local firing of dormant origins that rescue arrested forks. In sen1 mutants the MRX and Mrc1/Ctf4-complexes protect those forks clashing with transcription by preventing genotoxic fork-resection events mediated by the Exo1 nuclease. Hence, sister forks within the same replicon remain coupled when one of the two forks halts. This is different when forks encounter double strand breaks. Moreover, the local firing of dormant origins is not prevented by checkpoint activation but depends on delayed adjacent forks. Furthermore, a productive head-on clash between replication and transcription requires the tuning of origin firing and coordination between Sen1, the MRX and Mrc1/Ctf4-complexes and Exo1.

2017-10-11 | GSE97046 | GEO