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:Deposition of histone H3 lysine 4 (H3K4) methylation at promoter regions by the SET1/COMPASS complex is associated with context-dependent effects on gene expression. Transcription-independent functions have also been attributed to this highly conserved complex, but whether these contribute to higher-order chromosome organization has not been explored. Using a quantitative FRET (Förster resonance energy transfer)-based fluorescence lifetime imaging microscopy (FLIM) approach to assay nanometer scale chromatin compaction in live animals, we reveal an unexpected role for SET1/COMPASS in structuring meiotic chromosomes in the germline of C. elegans. Inactivation of SET-2, the C. elegans homologue of the catalytic subunit SET1, strongly enhanced chromosome organization defects and loss of fertility resulting from partial depletion of condensin-II. Loss of CFP-1, the chromatin targeting subunit of COMPASS, similarly affected germline chromatin compaction measured by FLIM-FRET and enhanced condensin-II knock-down phenotypes. Defects in chromosome morphology following conditional inactivation of topoisomerase II, another structural component of chromosomes, were also aggravated in the absence of set-2. Our results are consistent with a role of SET1/COMPASS in shaping meiotic chromosomes in the C. elegans germline, and have important implications for how chromatin-modifying complexes and histone modifications may cooperate with non histone-proteins to achieve proper chromosome organization, not only in meiosis, but also in mitosis.
2020-09-03 | GSE146932 | GEO
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.
2019-12-17 | GSE129928 | GEO
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.
2020-09-14 | GSE143338 | GEO
Project description:Deposition of histone H3 lysine 4 (H3K4) methylation at promoters is catalyzed by the SET1/COMPASS complex and is associated with context-dependent effects on gene expression and local changes in chromatin organization. The role of SET1/COMPASS in shaping chromosome architecture has not been investigated. Here we used Caenorhabditis elegans to address this question through a live imaging approach and genetic analysis. Using quantitative FRET (Förster resonance energy transfer)-based fluorescence lifetime imaging microscopy (FLIM) on germ cells expressing histones eGFP-H2B and mCherry-H2B, we find that SET1/COMPASS influences meiotic chromosome organization, with marked effects on the close proximity between nucleosomes. We further show that inactivation of set-2, encoding the C. elegans SET1 homologue, or CFP-1, encoding the chromatin targeting subunit of COMPASS, enhances germline chromosome organization defects and sterility of condensin-II depleted animals. set-2 loss also aggravates germline defects resulting from conditional inactivation of topoisomerase II, another structural component of chromosomes. Expression profiling of set-2 mutant germlines revealed only minor transcriptional changes, suggesting that the observed effects are at least partly independent of transcription. Altogether, our results are consistent with a role for SET1/COMPASS in shaping meiotic chromosomes in C. elegans, together with the non-histone proteins condensin-II and topoisomerase. Given the high degree of conservation, our findings expand the range of functions attributed to COMPASS and suggest a broader role in genome organization in different species.
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Project description:CTCF is present at the anchors of thousands of loops likely formed via cohesin-mediated loop extrusion in mammalian cells. Interaction domains present in D. melanogaster chromosomes form via the segregation of active and inactive chromatin in the absence of CTCF looping, but the role of transcription versus other architectural proteins in chromatin organization is unclear. Here we find that positioning of RNAPII via transcription elongation is essential in the formation of gene loops, which in turn interact to form compartmental domains. Inhibition of transcription elongation or depletion of cohesin decreases gene looping and formation of active compartmental domains. In contrast, depletion of condensin II, which also localizes to active chromatin, results in increased gene looping, formation of compartmental domains, and stronger intra-chromosomal compartmental interactions. Condensin II has a similar role in maintaining inter-chromosomal interactions responsible for pairing between homologous chromosomes, whereas inhibition of transcription elongation or cohesin depletion has little effect on homolog pairing. The results suggest distinct roles for cohesin and condensin II in the establishment of 3D nuclear organization in Drosophila.
2019-03-11 | GSE118756 | GEO
Project description:Dosage compensation in Caenorhabditis elegans equalizes X-linked gene expression between XX hermaphrodites and XO males. The process depends on a condensin-containing dosage compensation complex (DCC), which binds the X chromosomes in hermaphrodites to repress gene expression. Condensin IDC and an additional five DCC components must be present on the X during early embryogenesis in hermaphrodites to establish dosage compensation. However, whether the DCC's continued presence is required to maintain the repressed state once established is unknown. Beyond the role of condensin IDC in X chromosome compaction, additional mechanisms contribute to X-linked gene repression. DPY-21, a non-condensin IDC DCC component, is an H4K20me2/3 demethylase whose activity enriches the repressive histone mark, H4 lysine 20 monomethylation on the X chromosomes. In addition, CEC-4 tethers H3K9me3-rich chromosomal regions to the nuclear lamina, which also contributes to X-linked gene repression. To investigate the necessity of condensin IDC during the larval and adult stages of hermaphrodites, we used the auxin-inducible degradation system to deplete the condensin IDC subunit DPY-27. While DPY-27 depletion in the embryonic stages resulted in lethality, DPY-27 depleted larvae and adults survive. In these DPY-27 depleted strains, condensin IDC was no longer associated with the X chromosome, the X became decondensed, and the H4K20me1 mark was gradually lost, leading to X-linked gene derepression. These results suggest that the stable maintenance of dosage compensation requires the continued presence of condensin IDC. A loss-of-function mutation in cec-4, in addition to the depletion of DPY-27 or the genetic mutation of dpy-21, led to even more significant increases in X-linked gene expression, suggesting that tethering heterochromatic regions to the nuclear lamina helps stabilize repression mediated by condensin IDC and H4K20me1.
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Project description:Condensin I and Condensin II promote drastic spatial compaction (condensation) of the genome upon mitotic entry. Condensin I binds chromatin only after dissolution of the nuclear envelope in prophase. Conversely, Condensin II is nuclear throughout the cell cycle and initiates chromosome condensation. Previous studies demonstrated that MCPH1 inhibits Condensin II to prevent chromosome condensation during interphase. Mechanisms that promote Condensin II activation in early mitosis likely exist but are currently unknown. Through genetic and proteomic approaches, we identify M18BP1, a protein previously associated with centromere identity, as a factor required for Condensin II localization to chromatin during mitosis. To activate and localize Condensin II, M18BP1 directly binds the CAP-G2 subunit. M18BP1 and MCPH1 compete for CAP-G2 binding, and CDK1 phosphorylation promotes replacement of MCPH1 with M18BP1 to activate Condensin II upon mitotic entry. Our results identify a fundamental and evolutionarily conserved mechanism of Condensin II activation
2025-11-03 | PXD051556 | Pride
Project description:Condensin I and condensin II promote drastic spatial compaction (condensation) of the genome upon mitotic entry. Condensin I binds chromatin only after dissolution of the nuclear envelope in prophase. Conversely, condensin II is nuclear throughout the cell cycle and initiates chromosome condensation. Previous studies demonstrated that MCPH1 inhibits condensin II to prevent chromosome condensation during interphase. Mechanisms that promote condensin II activation in early mitosis likely exist but are currently unknown. Through genetic and proteomic approaches, we identify M18BP1, a protein previously associated with centromere identity, as a factor required for condensin II localization to chromatin during mitosis. To activate and localize condensin II, M18BP1 directly binds the CAP-G2 subunit. M18BP1 and MCPH1 compete for CAP-G2 binding, and CDK1 phosphorylation promotes replacement of MCPH1 with M18BP1 to activate condensin II upon mitotic entry. Our results identify a fundamental and evolutionarily conserved mechanism of condensin II activation.
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