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Transcription-dependent positioning of Structural Maintenance of Chromosome complexes across the genome: RNA-Seq

ABSTRACT: The Structural Maintenance of Chromosomes (SMC) complexes regulate the chromosome structures essential for proper genome regulation and cell viability. In mammals, the coordinated actions of the SMC complexes condensin I, condensin II and cohesin regulate dynamic chromosome structures throughout the cell cycle, but it is not clear how these complexes are positioned across the genome. We report here that condensin I, condensin II and cohesin occupy active euchromatic regions of the embryonic stem cell genome, but not heterochromatic regions. Like cohesin, we find that condensin II is deposited at active genes by the SMC loading factor Nipbl. The recruitment of Condensin II to active genes is dependent on their transcriptional activation. Subsequent transcriptional elongation by RNA polymerase II distributes condensin II across gene bodies. During mitosis, condensin I occupies the same set of active genes occupied by condensin II during interphase. Thus, SMC complexes are positioned in the genome by transcription-dependent processes, indicating that condensin-dependent condensation mechanisms are preferentially utilized in euchromatic regions. RNA-seq in mES cells after known-down of Smc1, CapH2 or Smc2.

ORGANISM(S): Mus musculus

SUBMITTER: Richard Young

PROVIDER: E-GEOD-46316 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcription-dependent positioning of Structural Maintenance of Chromosome complexes across the genome: RNA-Seq

Project description:The Structural Maintenance of Chromosomes (SMC) complexes regulate the chromosome structures essential for proper genome regulation and cell viability. In mammals, the coordinated actions of the SMC complexes condensin I, condensin II and cohesin regulate dynamic chromosome structures throughout the cell cycle, but it is not clear how these complexes are positioned across the genome. We report here that condensin I, condensin II and cohesin occupy active euchromatic regions of the embryonic stem cell genome, but not heterochromatic regions. Like cohesin, we find that condensin II is deposited at active genes by the SMC loading factor Nipbl. The recruitment of Condensin II to active genes is dependent on their transcriptional activation. Subsequent transcriptional elongation by RNA polymerase II distributes condensin II across gene bodies. During mitosis, condensin I occupies the same set of active genes occupied by condensin II during interphase. Thus, SMC complexes are positioned in the genome by transcription-dependent processes, indicating that condensin-dependent condensation mechanisms are preferentially utilized in euchromatic regions.

2013-10-28 | GSE46316 | GEO

Transcription-associated Loading and Translocation of Condensin II on Chromosome Arms in Embryonic Stem Cells (flavopiridol ChIP-Seq)

Project description:Condensin molecules are loaded onto the genome to mediate essential changes in chromosome condensation during mitosis, but it is not clear why there are two forms of vertebrate condensin that become differentially distributed on chromosomes. We report here that condensin II, the form of condensin present in the nucleus throughout the cell cycle, functions specifically at active genes. Condensin II is loaded at transcriptionally active promoters in embryonic stem cells (ESCs), migrates through these genes in a transcription-dependent fashion and accumulates in transcription termination regions. Unlike cohesin, which is also loaded at active promoters, condensin II has little influence on transcription. We conclude that condensin II is loaded and distributed across actively transcribed chromatin and thus serves to specifically condense this euchromatic portion of chromosomes during the cell division cycle. ChIP-Seq data for Condensin II and Cohesin in v6.5 ESCs treated or not with the RNA polymerase II elongation inhibitor flavopiridol.

2012-02-09 | E-GEOD-30919 | biostudies-arrayexpress

Bacillus subtilis SMC complexes juxtapose chromosome arms as they travel from origin to terminus

Project description:Structural maintenance of chromosomes (SMC) complexes play critical roles in chromosome dynamics in virtually all organisms but how they function remains poorly understood. In Bacillus subtilis, SMC condensin complexes are topologically loaded at centromeric sites adjacent to the replication origin. Here we provide evidence that these ring-shaped assemblies tether the left and right chromosome arms together while traveling from the origin to the terminus (>2 Mb) at rates >50kb/min. Condensin movement scales linearly with time arguing for an active transport mechanism. These data support a model in which SMC complexes function by processively enlarging DNA loops. Loop formation followed by processive enlargement provides a mechanism for how condensin complexes compact and resolve sister chromatids in mitosis and how cohesin generates topologically associating domains (TADs) during interphase.

2017-02-03 | GSE85612 | GEO

SMC Complexes Are Guarded by the SUMO Protease Ulp2 Against SUMO-Chain-Mediated Turnover

Project description:Structural maintenance of chromosomes (SMC) complexes, cohesin, condensin and Smc5/6, are essential for viability and participate in multiple processes, including sister chromatid cohesion, chromosome condensation, and DNA repair. Here we show that SUMO chains target all three SMC complexes and are antagonized by the SUMO protease Ulp2 to prevent their turnover. We uncover that the essential role of the cohesin-associated subunit Pds5 is to counteract SUMO chains jointly with Ulp2. Importantly, fusion of Ulp2 to kleisin Scc1 supports viability of PDS5 null cells and protects cohesin from proteasomal degradation mediated by the SUMO-targeted ubiquitin ligase Slx5/Slx8. The lethality of PDS5 deleted cells can also be bypassed by simultaneous loss of the PCNA unloader, Elg1, and the cohesin releaser, Wpl1, but only when Ulp2 is functional. Condensin and Smc5/6 complex are similarly guarded by Ulp2 against unscheduled SUMO-chain assembly, which we propose to time the availability of SMC complexes on chromatin.

2021-08-05 | PXD022717 | Pride

Sister chromatid cohesion halts DNA loop expansion

Project description:Eukaryotic genomes are folded into DNA loops mediated by SMC complexes, like cohesin, condensin and Smc5/6. This organization regulates different DNA related processes along the cell cycle such as transcription, recombination, segregation and DNA repair. During G2/M phases, SMC complexes mediated DNA loops coexist with cohesin complexes involved in sister chromatid cohesion (SCC). It remains unknown whether SCC and DNA loop expansion influence each other and if they cooperate to regulate DNA-related processes. Here we show that SCC is indeed a barrier to DNA loop expansion mediated by cohesin in G2.

2024-01-30 | GSE237031 | GEO

Selective compartmentalization in condensin-depleted mitotic chromosomes

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

Condensin I folds the C. elegans genome [RNA-seq]

Project description:Structural Maintenance of chromosomes (SMC) complexes, cohesin and condensins, have been named after their roles during meiosis and mitosis. Recent data in mammalian cells and Drosophila have described the additional role of cohesin for genome folding into loops and domains during interphase. However, determinants of genome folding in holocentric species remain unclear. Using high resolution chromosome conformation capture, we show that overlapping large-scale nuclear localization and small-scale epigenomic states compartmentalize the C. elegans genome. By systematically and acutely inactivating each SMC complex, we observe that in contrast to other studied systems, cohesin creates small loops, while condensin I has a major role in genome folding: its inactivation causes genome-wide decompaction, chromosome mixing, loss of loops and TAD structures and reinforcement of fine-scale epigenomic compartments. Counter-intuitively, removal of condensin I and its X-specific variant condensin IDC from the X chromosomes led to the formation of a loop compartment coinciding with a subset of previously characterized loading sites for condensin IDC and bound by the X-targeting complex SDC. While transcriptional changes were limited for all autosomes upon cohesin and condensin II inactivation, removal of condensin I/IDC from the X chromosome led to transcriptional up-regulation of X-linked genes demonstrating that a sustained role for condensin IDC in gene regulation. Finally, while condensin I inactivation leads to reduced lifespan, we show that this reduction is due to X-specific gene upregulation rather than global genome decompaction.

2024-04-18 | GSE199717 | GEO

Condensin I folds the C. elegans genome [Hi-C]

2024-04-18 | GSE199721 | GEO

Condensin I folds the C. elegans genome [Ribo-Zero-seq]

2024-04-18 | GSE199719 | GEO

SMC5/6 facilitates joint molecule resolution and stepwise loss of cohesin to promote meiotic chromosome segregation

Project description:During meiosis, Structural Maintenance of Chromosome (SMC) complexes underpin two fundamental features of meiosis: homologous recombination and chromosome segregation. While meiotic functions of the cohesin and condensin complexes have been delineated, the role of the third SMC complex, Smc5/6, remains enigmatic. Diminished Smc5/6 function causes severe defects in nuclear division, but the underlying causes of these defects remain unclear. Here we identify specific, essential meiotic functions for the Smc5/6 complex in homologous recombination and regulation of cohesin. We show that Smc5/6 is enriched at centromeres and cohesin-association sites where it regulates sister-chromatid cohesion and the timely removal of cohesin from chromosomal arms, respectively. Smc5/6 also localizes to recombination hotspots, where it promotes normal formation and resolution of joint-molecule intermediates. Furthermore, we find that Smc5/6 specifically promotes resolution of joint molecules via the XPF-family endonuclease, Mus81-Mms4Eme1. We propose that Smc5/6 acts as a chaperone for M-bM-^@M-^XmitoticM-bM-^@M-^Y-like recombination processes during meiosis. ChIP-chip was used to compare Smc5 localization in wild-type and spo11 strains

2013-12-27 | E-GEOD-44852 | biostudies-arrayexpress

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