Condensin Accelerates Long-Range Intra-Chromosomal Interactions
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1258174 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33410846_1.fastq.gz | Fastqsanger.gz | |||
| SRR33410846_2.fastq.gz | Fastqsanger.gz | |||
| SRR33410847_1.fastq.gz | Fastqsanger.gz | |||
| SRR33410847_2.fastq.gz | Fastqsanger.gz | |||
| SRR33410848_1.fastq.gz | Fastqsanger.gz |
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Project description:The 3D genome organization plays a key role in regulating interactions among chromosomal loci. While Chromosome Conformation Capture (3C)-based methods have provided static snapshots of chromatin architecture, the kinetics of chromosomal encounters in live cells remain poorly characterized. In this study, we employ Chemically Induced Chromosomal Interaction (CICI) to measure encounter times between multiple loci pairs in G1-arrested budding yeast. Our results show that chromosome motion closely follows the Rouse polymer model, with similar diffusion parameters at all tested loci. Surprisingly, we find that long-range intra-chromosomal encounters occur significantly faster than inter-chromosomal encounters at similar 3D distances. Using targeted depletion experiments, we identify condensin, but not cohesin, as the complex responsible for these rapid intra-chromosomal interactions. This is further supported by Hi-C analysis, which reveals that condensin promotes long-distance intra-chromosomal interactions in G1 yeast. Through polymer simulations, we estimate that condensin extrudes chromatin at ~2 kb/s with a density of one complex per 1-2 Mb and a processivity of 120-220 kb. These findings uncover a novel role for condensin in shaping the interphase genome organization and provide new insights into chromosomal search dynamics in vivo.
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Project description:Chromosomal translocations play pivotal roles in various physiological and pathological processes, such as immunoglobulin production and tumor progression; however, the infrequency of chromosomal translocation events has impeded the exploration of the underlying mechanisms. To tackle this challenge, we devised a strategy to report and enrich cells with translocations in vitro, in conjunction with a novel method termed High Multiplex Translocation Sequencing (HMTS), to capture genome-wide translocations from multiple bait regions simultaneously. Analysis of HMTS data unveiled a preference for translocations to occur at Topologically Associating Domain (TAD) boundaries, and experimental disruption of the TAD boundary indeed led to a reduction in translocation frequency, exemplified by translocations involving ERG. Knockdown of Cohesin or condensin II was observed distinct roles in translocations. Cohesin deficiency promoted long-distance translocations, while condensin II deficiency promoted short distance translocation, inside TAD, and decreased intra-chromatin long-distance translocation, particularly at TAD boundaries. For inter-chromatin, although condensin II deficiency also decreased the translocation at TAD boundaries, and highly transcription regions while paradoxically slightly increased inter-chromatin translocation ratio, suggesting that condensin II physiologically mediated inter-chromatin interaction at TAD boundary regions but simultaneously restricted interaction from other regions, such as centromere. Our new translocation sequencing method revealed the versatile role of condensin II in controlling intra-chromatin short-distance, long-distance, and inter-chromosome translocations.
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Project description:Antibody class switch recombination (CSR) in B lymphocytes joins two DNA double-strand breaks (DSBs) lying 100 to 200 kilobases (kb) apart within switch (S) regions in the immunoglobulin heavy chain locus (IgH). CSR-activated B lymphocytes generate multiple S-region DSBs in the donor Sm and in a downstream acceptor S region, with a DSB in Sm being joined to a DSB in the acceptor S region at sufficient frequency to drive CSR in a large fraction of activated B cells. Such frequent joining of widely separated CSR DSBs could be promoted by IgH-specific or B cell-specific processes or by general aspects of chromosome architecture and DSB repair. Previously, we found that B cells with two yeast I-SceI endonuclease targets in place of Sg1 undergo I-SceI-dependent class switching from IgM to IgG1 at 5-10% of normal levels. Now, we report that B cells in which Sg1 is replaced with a 28 I-SceI target array, designed to increase I-SceI DSB frequency, undergo I-SceI-dependent class switching at almost normal levels. High-throughput genome-wide translocation sequencing revealed that I-SceI-generated DSBs introduced in cis at Sm and Sg1 sites are joined together in T cells at levels similar to those of B cells. Such high joining levels also occurred between I-SceI-generated DSBs within c-myc and I-SceI- or CRISPR/Cas9-generated DSBs 100 kb downstream within Pvt1 in B cells or fibroblasts, respectively. We suggest that CSR exploits a general propensity of intra-chromosomal DSBs separated by several hundred kb to be frequently joined together and discuss relevance of this finding for recurrent interstitial deletions in cancer. Comparison of frequency of long-range joining between I-SceI-induced DSBs at IgH and c-myc loci in different cell types by HTGTS
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Project description:Faithful chromosome segregation requires packaging of the genome on both global and local scales. Condensin plays a crucial role at pericentromeres to resist spindle forces and ensure the oriented attachment of kinetochores to microtubules at mitosis. Here we demonstrate that budding yeast condensin is recruited to pericentromeres through a direct interaction between its Ycg1 subunit and the pericentromeric adaptor protein, shugoshin (Sgo1). We identify a Short Linear Motif (SLiM), termed CR1, within the C-terminal region of Sgo1 which inserts into a conserved pocket on Ycg1. Disruption of this interface abolishes the Sgo1-condensin interaction, prevents condensin recruitment to pericentromeres and results in defective sister kinetochore biorientation in mitosis. Similar motifs to CR1 are found in known and potential condensin binding partners and the Ycg1 binding pocket is broadly conserved, including in mammalian CAP-G proteins. Overall, we uncover the molecular mechanism that targets condensin to define a specialized chromosomal domain.
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Project description:ARID1A regulates condensin II distribution and chromosomal partition
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Project description:ARID1A, a subunit of the switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex, influences gene accessibility. However, the role of ARID1A in spatial genomic organization and chromosomal interaction remains elusive. We showed that the SWI/SNF complex interacts with condensin II and they show significant overlapping distributions in enhancers. ARID1A inactivation drives redistribution of condensin II preferentially at enhancers without affecting the interaction between the SWI/SNF and condensing II complexes. ARID1A and condensin II contribute to transcriptionally inactive B compartments, while ARID1A weakens the borders of topologically associated domains. ARID1A inactivation decreases the frequency of genomic interactions over distance, but increases the intermixing of interphase small chromosomes, which was validated by three dimensional chromosome painting. These results demonstrated ARID1A spatially partitions genome and chromosomes.
2019-05-21 | GSE120059 | GEO
Project description:ARID1A, a subunit of the switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex, influences gene accessibility. However, the role of ARID1A in spatial genomic organization and chromosomal interaction remains elusive. We showed that the SWI/SNF complex interacts with condensin II and they show significant overlapping distributions in enhancers. ARID1A inactivation drives redistribution of condensin II preferentially at enhancers without affecting the interaction between the SWI/SNF and condensing II complexes. ARID1A and condensin II contribute to transcriptionally inactive B compartments, while ARID1A weakens the borders of topologically associated domains. ARID1A inactivation decreases the frequency of genomic interactions over distance, but increases the intermixing of interphase small chromosomes, which was validated by three dimensional chromosome painting. These results demonstrated ARID1A spatially partitions genome and chromosomes.
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Project description:ARID1A, a subunit of the switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex, influences gene accessibility. However, the role of ARID1A in spatial genomic organization and chromosomal interaction remains elusive. We showed that the SWI/SNF complex interacts with condensin II and they show significant overlapping distributions in enhancers. ARID1A inactivation drives redistribution of condensin II preferentially at enhancers without affecting the interaction between the SWI/SNF and condensing II complexes. ARID1A and condensin II contribute to transcriptionally inactive B compartments, while ARID1A weakens the borders of topologically associated domains. ARID1A inactivation decreases the frequency of genomic interactions over distance, but increases the intermixing of interphase small chromosomes, which was validated by three dimensional chromosome painting. These results demonstrated ARID1A spatially partitions genome and chromosomes.
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Project description:ARID1A regulates condensin II distribution and chromosomal partition [HiC]
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Project description:Faithful chromosome segregation requires packaging of the genome on both global and local scales. Condensin plays a crucial role at pericentromeres to resist spindle forces and ensure the oriented attachment of kinetochores to microtubules at mitosis. Here we demonstrate that budding yeast condensin is recruited to pericentromeres through a direct interaction between its Ycg1 subunit and the pericentromeric adaptor protein, shugoshin (Sgo1). We identify a Short Linear Motif (SLiM), termed CR1, within the C-terminal region of Sgo1 which inserts into a conserved pocket on Ycg1. Disruption of this interface abolishes the Sgo1-condensin interaction, prevents condensin recruitment to pericentromeres and results in defective sister kinetochore biorientation in mitosis. Similar motifs to CR1 are found in known and potential condensin binding partners and the Ycg1 binding pocket is broadly conserved, including in mammalian CAP-G proteins. Overall, we uncover the molecular mechanism that targets condensin to define a specialized chromosomal domain.
2024-12-10 | PXD056626 | Pride