RNA Pol II transcription antagonises mitotic chromosome assembly and segregation by condensin
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ABSTRACT:
PROVIDER: PRJNA990749 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25118718_1.fastq.gz | Fastqsanger.gz | |||
| SRR25118718_2.fastq.gz | Fastqsanger.gz | |||
| SRR25118719_1.fastq.gz | Fastqsanger.gz | |||
| SRR25118719_2.fastq.gz | Fastqsanger.gz | |||
| SRR25118720_1.fastq.gz | Fastqsanger.gz |
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Project description:Condensin drives mitotic chromosome assembly by folding chromatin into loops and is enriched in the vicinity of highly expressed genes, but the significance of such proximity with respect to condensin activity has remained unclear. Here, by modulating the occupancy of RNA Pol II in vivo, we show that transcription plays no role in the steady state association of condensin with DNA. Rather, transcription stalls and even displaces condensin, hindering its ability to fold chromatin and to support chromosome segregation. Our results highlight a key aspect of the integrated functioning of condensin and suggest that a tight control of transcription underlies mitotic chromosome assembly.
2024-02-03 | GSE236395 | GEO
Project description:Genome/chromosome organization is highly ordered and controls nuclear events. Here, we show that the TATA box-binding protein (TBP) interacts with the Cnd2 kleisin subunit of condensin to mediate interphase and mitotic chromosome organization in fission yeast. TBP recruits condensin onto RNA polymerase III-transcribed (Pol III) genes and highly transcribed Pol II genes; condensin in turn associates these genes with centromeres. Inhibition of the Cnd2-TBP interaction disrupts condensin localization across the genome and the proper assembly of mitotic chromosomes, leading to severe defects in chromosome segregation and eventually causing cellular lethality. We propose that the Cnd2-TBP interaction coordinates transcription with chromosomal architecture by linking dispersed gene loci with centromeres. This chromosome arrangement can contribute to the efficient transmission of physical force at the kinetochore to chromosomal arms, thereby supporting the fidelity of chromosome segregation. Genome-wide distributions of condensin and Pol III factors in fission yeast.
2015-08-12 | E-GEOD-60273 | biostudies-arrayexpress
Project description:Genome/chromosome organization is highly ordered and controls nuclear events. Here, we show that the TATA box-binding protein (TBP) interacts with the Cnd2 kleisin subunit of condensin to mediate interphase and mitotic chromosome organization in fission yeast. TBP recruits condensin onto RNA polymerase III-transcribed (Pol III) genes and highly transcribed Pol II genes; condensin in turn associates these genes with centromeres. Inhibition of the Cnd2-TBP interaction disrupts condensin localization across the genome and the proper assembly of mitotic chromosomes, leading to severe defects in chromosome segregation and eventually causing cellular lethality. We propose that the Cnd2-TBP interaction coordinates transcription with chromosomal architecture by linking dispersed gene loci with centromeres. This chromosome arrangement can contribute to the efficient transmission of physical force at the kinetochore to chromosomal arms, thereby supporting the fidelity of chromosome segregation.
2015-08-12 | GSE60273 | GEO
Project description:Chromatin fibres dynamically change their organisation during cell cycle. In interphase nucleus, chromatin fibres are evenly distributed whereas their spatial occupancy are reorganised to form condensed chromosomes in mitosis. This process called chromosome condensation is necessary for an accomplishment of faithful chromosome segregation. One of the Structural Maintenance of Chromosomes complexes, Condensin, is indispensable for chromosome condensation. It remains, however, unknown how Condensin plays its role in shaping mitotic chromosome. Here we show that chromatin fibres change their interacting partners; short-range contacts in interphase nucleus are converted into long-range interactions to shape condensed chromosomes. This conversion of interactions among chromatin fibres results in the formation of larger domains within mitotic chromosomes. Condensin is solely in charge of the conversion and large domain formation in fission yeast mitosis. Our results show how fission yeast Condensin is involved in shaping mitotic chromosomes.
2017-07-13 | GSE94474 | GEO
Project description:Chromatin fibres dynamically change their organisation during cell cycle. In interphase nucleus, chromatin fibres are evenly distributed whereas their spatial occupancy are reorganised to form condensed chromosomes in mitosis. This process called chromosome condensation is necessary for an accomplishment of faithful chromosome segregation. One of the Structural Maintenance of Chromosomes complexes, Condensin, is indispensable for chromosome condensation. It remains, however, unknown how Condensin plays its role in shaping mitotic chromosome. Here we show that chromatin fibres change their interacting partners; short-range contacts in interphase nucleus are converted into long-range interactions to shape condensed chromosomes. This conversion of interactions among chromatin fibres results in the formation of larger domains within mitotic chromosomes. Condensin is solely in charge of the conversion and large domain formation in fission yeast mitosis. Our results show how fission yeast Condensin is involved in shaping mitotic chromosomes.
2017-07-13 | GSE94475 | GEO
Project description:ABSTRACT: Condensin is a central regulator of mitotic genome structure, with mutants showing poorly condensed chromosomes and profound segregation defects. Here we identify the fission yeast NCT complex, comprising the Nrc1 BET-family tandem bromodomain protein (SPAC631.02), Casein Kinase II (CKII) and several TAFs, as a novel regulator of condensin function (where NCT mutants restore the formation of segregation-competent chromosomes in cells containing defective condensin). Synchronous ChIP-seq shows that NCT and condensin bind similar genomic regions, but only briefly co-localize during the periods of chromosome condensation and decondensation. These results are consistent with a model where NCT targets CKII to chromatin in a cell cycle-directed manner to modulate the activity of condensin during chromosome condensation and decondensation. DATA: Study includes ChIP-seq of fission yeast H3-K4Me3, H3-K36Me3, TBP, Taf7, Nrc1, Cka1 from aynchronous cells; Nrc1 and Cut3 (representing condensin) from four synchronized cell-cycle stages estimated as G2/M, Metaphase, Anaphase and G1/S.
2014-01-10 | E-GEOD-53955 | biostudies-arrayexpress
Project description:ABSTRACT: Condensin is a central regulator of mitotic genome structure, with mutants showing poorly condensed chromosomes and profound segregation defects. Here we identify the fission yeast NCT complex, comprising the Nrc1 BET-family tandem bromodomain protein (SPAC631.02), Casein Kinase II (CKII) and several TAFs, as a novel regulator of condensin function (where NCT mutants restore the formation of segregation-competent chromosomes in cells containing defective condensin). Synchronous ChIP-seq shows that NCT and condensin bind similar genomic regions, but only briefly co-localize during the periods of chromosome condensation and decondensation. These results are consistent with a model where NCT targets CKII to chromatin in a cell cycle-directed manner to modulate the activity of condensin during chromosome condensation and decondensation.
2014-01-10 | GSE53955 | GEO
Project description:During the G2/M transition, SMC protein complexes including extrusive-cohesin, cohesive-cohesin and condensin are co-present on the chromatin. Yet, the precise pattern of interactions among these complexes and the subsequent impact on chromatin architecture remain elusive. Here, we utilize mitotic chromosome as a unified experimental platform to dissect their rules of engagement. We find that condensin disrupts the focal binding of both extrusive- and cohesive-cohesin, leading to disassembly of TADs and loops. Reciprocally, both extrusive- and cohesive-cohesin affect condensin activity and mitotic chromosome organization. Extrusive-cohesin impairs chromosome helicity and cohesive-cohesin reduces helical layer size. In the absence of condensin, extrusive-cohesin establishes TADs and loops. Conversely, cohesive-cohesin by itself does not induce these structures, nor does it form independent peaks, suggesting lack of extruding activity. Instead, cohesive-cohesin modulates pre-existing TADs and loops, intensifying intra-TAD interactions while restricting loop expansion. Collectively, our data reveal a tripartite interplay among extrusive-cohesin, cohesive-coheisn and condensin that dynamically sculpts chromatin architecture during mitotic progression
2024-12-21 | GSE269952 | GEO
Project description:Condensin plays fundamental roles in chromosome dynamics. In this study, we determined the binding sites of condensin on fission yeast (Schizosaccharomyces pombe) chromosomes at the level of nucleotide sequences using chromatin immunoprecipitation (ChIP) and ChIP-sequencing (ChIP-seq). We found that condensin binds to RNA polymerase I-, II- and III-transcribed genes during both mitosis and interphase, and we focused on pol II constitutive and inducible genes. Accumulation sites for condensin are distinct from those of cohesin and DNA topoisomerase II. Using cell cycle stage- and heat shock-inducible genes, we demonstrate that pol II-mediated transcripts cause condensin accumulation. First, condensin’s enrichment on mitotically activated genes was abolished by deleting the sep1+ gene that encodes an M-phase-specific forkhead transcription factor. Second, by raising the temperature, condensin accumulation was rapidly induced at heat shock protein genes in interphase and even during mid-mitosis. In interphase, condensin accumulates preferentially during the post-replicative phase. pol II-mediated transcription was neither repressed nor activated by condensin, as levels of transcripts per se did not change when mutant condensin failed to associate with chromosomal DNA. However, massive chromosome missegregation occurred, suggesting that abundant pol II transcription may require active condensin prior to proper chromosome segregation.
2015-04-15 | GSE65956 | GEO
Project description:During mitosis, condensin activity is thought to disrupt interphase chromatin structures. Here, we utilize condensin-deficient mitotic chromosomes as a unique architectural platform to further investigate genome folding principles. Upon condensin loss, compartments progressively emerge in mitotic chromosomes. Euchromatin diverges into two different compartments A1 and A2, the former of which shows strong homotypic interactions while the latter exhibit reduced self-aggregation. Constitutive heterochromatin (B1) displays reduced level of compartmentalization and the normally inert facultative heterochromatin (B2) participates to compartmentalize the genome. Dynamically, A1 compartment is established remarkably fast with similarly efficient separation from B1 while reformation of B1 is delayed, implying that A1 self-attraction is the engine to compartmentalizalize the condensin-depleted mitotic chromosomes. Notified by the mitotic compartmentalization of B1 which lacks HP1 binding, we sought to explore the role of HP1 proteins in genome folding and demonstrat that HP1& are dispensible for chromatin structural restoration during cell divison. Our observations unveil delicate patterns and novel principles of genome compartmentalization that are otherwise hidden in interphase cells.
2023-11-22 | GSE228160 | GEO