Cooperation between Caenorhabditis elegans COMPASS and condensin in germline chromatin organization
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA612496 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11305058.fastq.gz | Fastqsanger.gz | |||
| SRR11305059.fastq.gz | Fastqsanger.gz | |||
| SRR11305060.fastq.gz | Fastqsanger.gz | |||
| SRR11305061.fastq.gz | Fastqsanger.gz | |||
| SRR11305062.fastq.gz | Fastqsanger.gz |
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Project description:Chromatin state influences lifespan and may allow for the epigenetic inheritance of this complex trait. At sites of active transcription, the COMPASS complex methylates histone H3 at lysine 4 (H3K4me). In Caenorhabditis elegans, reductions in COMPASS extend lifespan, and wild-type descendants of COMPASS mutants inherit longevity for four generations. Here we show that the longevity of COMPASS mutants is itself a transgenerational trait caused by gradual changes in the repressive chromatin factor H3K9me2. H3K9me2 is required for longevity in COMPASS mutants and can confer longevity when increased in other chromatin modifier mutants. H3K9me2 levels also correlate with a transgenerational decline in wild-type lifespan after freezing or starvation. We propose that germline transcription-coupled H3K4me encroaches on H3K9me2 to limit lifespan. Loss of COMPASS complex alleviates the burden of H3K4me and therefore extends lifespan. This study suggests a causal role for a single heterochromatin factor in the establishment and inheritance of longevity.
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Project description:Prostate carcinoma (PCa) is the most common cancer of men, associated with a still unresolved issue of accurate risk-stratification. While recent advances in omics technologies have provided clues as to how molecular changes shape the onset and progression of PCa, it remains unclear whether germline variants and somatic mutations cooperate to contribute to PCa progression and outcome. Thus, we explored whether oncogenic cooperation between regulatory germline variants and somatic driver mutations may help explain why some PCa patients develop a more aggressive phenotype, which may have implications for risk-adapted medical treatment. We discovered PTPRK receptor-type protein-tyrosine phosphatase kappa (PTPRK) as a TMPRSS2::ERG (TE)-modulated gene associated with PCa progression whose expression is controlled by cooperation of the TE-fusion with a regulatory single nucleotide polymorphism (SNP).
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Project description:Eukaryotic genomes are organized into layers of chromatin domains, such as topologically associating domains (TADs) and A/B compartments. TADs (i.e., cohesin-mediated chromatin domains) are restricted by CCCTC-binding factor (CTCF) and convergent genes in higher eukaryotes and fission yeast, respectively. However, molecular mechanisms underlying the formation of condensin-mediated chromatin domains remain largely unclear. Here, we investigate the role of newly identified interaction between the Cnd1 condensin and Pmc4 mediator subunits. We develop a condensin mutation, cnd1-K658E, that impairs the condensin-mediator interaction and find that this mutation diminishes condensin-mediated domains and causes defects in chromosomal segregation. The condensin-mediator interaction is involved in recruiting condensin to highly transcribed genes and mitotically activated genes, the latter of which demarcate condensin-mediated domains. Our study also predicted that the condensin-mediator interaction and its function in chromosomal segregation are potentially conserved in human cells. This study provides a novel insight into how genome-wide gene expression is connected to the mitotic chromosomal architecture via the condensin-mediator interaction.
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Project description:Eukaryotic genomes are organized into layers of chromatin domains, such as topologically associating domains (TADs) and A/B compartments. TADs (i.e., cohesin-mediated chromatin domains) are restricted by CCCTC-binding factor (CTCF) and convergent genes in higher eukaryotes and fission yeast, respectively. However, molecular mechanisms underlying the formation of condensin-mediated chromatin domains remain largely unclear. Here, we investigate the role of newly identified interaction between the Cnd1 condensin and Pmc4 mediator subunits. We develop a condensin mutation, cnd1-K658E, that impairs the condensin-mediator interaction and find that this mutation diminishes condensin-mediated domains and causes defects in chromosomal segregation. The condensin-mediator interaction is involved in recruiting condensin to highly transcribed genes and mitotically activated genes, the latter of which demarcate condensin-mediated domains. Our study also predicted that the condensin-mediator interaction and its function in chromosomal segregation are potentially conserved in human cells. This study provides a novel insight into how genome-wide gene expression is connected to the mitotic chromosomal architecture via the condensin-mediator interaction.
2026-01-27 | GSE270576 | GEO
Project description:Eukaryotic genomes are organized into layers of chromatin domains, such as topologically associating domains (TADs) and A/B compartments. TADs (i.e., cohesin-mediated chromatin domains) are restricted by CCCTC-binding factor (CTCF) and convergent genes in higher eukaryotes and fission yeast, respectively. However, molecular mechanisms underlying the formation of condensin-mediated chromatin domains remain largely unclear. Here, we investigate the role of newly identified interaction between the Cnd1 condensin and Pmc4 mediator subunits. We develop a condensin mutation, cnd1-K658E, that impairs the condensin-mediator interaction and find that this mutation diminishes condensin-mediated domains and causes defects in chromosomal segregation. The condensin-mediator interaction is involved in recruiting condensin to highly transcribed genes and mitotically activated genes, the latter of which demarcate condensin-mediated domains. Our study also predicted that the condensin-mediator interaction and its function in chromosomal segregation are potentially conserved in human cells. This study provides a novel insight into how genome-wide gene expression is connected to the mitotic chromosomal architecture via the condensin-mediator interaction.
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Project description:Background: Structural maintenance of chromosomes (SMC) complexes are central organizers of chromatin architecture throughout the cell cycle. The SMC family member condensin is best known for establishing long-range chromatin interactions in mitosis. These compact chromatin and create mechanically stable chromosomes. How condensin contributes to chromatin organization in interphase is less well understood. Results: Here, we use efficient conditional depletion of fission yeast condensin to determine its contribution to interphase chromatin organization. We deplete condensin in G2 arrested cells to preempt confounding effects from cell cycle progression without condensin. Genome-wide chromatin interaction mapping, using Hi-C, reveals condensin-mediated chromatin interactions in interphase that are qualitatively similar to those observed in mitosis, but quantitatively far less prevalent. Despite its low abundance, chromatin mobility tracking shows that condensin markedly confines interphase chromatin movements. Without condensin, chromatin behaves as an unconstrained Rouse polymer with excluded volume, while condensin constrains its mobility. Unexpectedly, we find that condensin is required during interphase to prevent ongoing transcription from eliciting a DNA damage response. Conclusions: In addition to establishing mitotic chromosome architecture, condensin-mediated long-range chromatin interactions contribute to shaping chromatin organization in interphase. The resulting structure confines chromatin mobility and protects the genome from transcription-induced DNA damage. This adds to the important roles of condensin in maintaining chromosome stability.
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Project description:Resolving complex topological structures at replication forks is essential for faithful DNA replication, yet the underlying mechanisms remain poorly understood. Evidence from diverse eukaryotes suggests that condensin – best known for driving chromosome condensation in mitosis – may also operate during S phase to alleviate torsional stress in cooperation with topoisomerases. Here, we show in budding yeast and human cells that condensin binds stressed replication forks, where it cooperates with topoisomerases I and II to promote nascent DNA resection and restart replication. Our data indicate that condensin acts together with topoisomerase I at reversed forks to convert positive supercoils into topological DNA structures that are relaxed by topoisomerase II, enabling fork restart. These findings reveal an evolutionarily conserved role for condensin in resolving topological constraints at arrested forks, reminiscent of its function in chromosome segregation, and suggest that this activity helps prevent the formation of toxic chromosome structures during fork arrest and reversal.
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Project description: Not available
| S-EPMC7565041 | biostudies-literature