Condensin IDC, H4K20me1, and perinuclear tethering maintain X chromosome repression in C. elegans
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ABSTRACT:
PROVIDER: PRJNA1091897 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28457511_1.fastq.gz | Fastqsanger.gz | |||
| SRR28457511_2.fastq.gz | Fastqsanger.gz | |||
| SRR28457512_1.fastq.gz | Fastqsanger.gz | |||
| SRR28457512_2.fastq.gz | Fastqsanger.gz | |||
| SRR28457513_1.fastq.gz | Fastqsanger.gz |
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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.
2025-01-25 | GSE262451 | GEO
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.
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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.
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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.
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Project description:Condensins are multi-subunit protein complexes that regulate chromosome structure throughout cell-cycle. Metazoans contain two types of condensin complexes (I and II) with essential and distinct functions. In C. elegans a third type of condensin (IDC) functions as part of the X chromosome dosage compensation complex1,2. We mapped genome-wide binding sites of the three condensin types in C. elegans embryos. Characteristics of condensin binding are similar between condensin types.
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Project description:Condensins are multi-subunit protein complexes that regulate chromosome structure throughout cell-cycle. Metazoans contain two types of condensin complexes (I and II) with essential and distinct functions. In C. elegans a third type of condensin (IDC) functions as part of the X chromosome dosage compensation complex1,2. We mapped genome-wide binding sites of the three condensin types in C. elegans embryos. Characteristics of condensin binding are similar between condensin types. ChIP-seq profiles of C. elegans subunits of the three condensins in 3-6 replicates from mixed stage embryos, controls are included, and RNA-Seq profiles of C. elegans in 5 replicates from mixed staged embryos. Additionally, ChIP-seq profiles of the condensin II subunit KLE-2 in 6 replicates from L3 with controls, and RNA-Seq profiles of KLE-2 mutants in 3 replicates each from L3.
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Project description:Analyze condensin binding by fluorescence recovery after photobleaching (FRAP) and chromatin immunoprecipitation followed by sequencing (ChIP-seq) in ATP hydrolysis mutant and in mutants that affect the level of histone H4K20 methylation and H4K16ac enrichment and depletion on the X chromosome. We have also performed Hi-C analysis to test how 3D DNA interactions mediated by condensin DC change in the catalytic and null mutant of dpy-21, a H4K20me2 demethylase that increase H4K20me1 on the X.
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Project description:analyze condensin binding by fluorescence recovery after photobleaching (FRAP) and chromatin immunoprecipitation followed by sequencing (ChIP-seq) in ATP hydrolysis mutant and in mutants that affect the level of histone H4K20 methylation and H4K16ac enrichment and depletion on the X chromosome. We have also performed Hi-C analysis to test how 3D DNA interactions mediated by condensin DC change in the catalytic and null mutant of dpy-21, a H4K20me2 demethylase that increase H4K20me1 on the X.
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Project description:Analyze condensin binding by fluorescence recovery after photobleaching (FRAP) and chromatin immunoprecipitation followed by sequencing (ChIP-seq) in ATP hydrolysis mutant and in mutants that affect the level of histone H4K20 methylation and H4K16ac enrichment and depletion on the X chromosome. We have also performed Hi-C analysis to test how 3D DNA interactions mediated by condensin DC change in the catalytic and null mutant of dpy-21, a H4K20me2 demethylase that increase H4K20me1 on the X.
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Project description:Analyze condensin binding by fluorescence recovery after photobleaching (FRAP) and chromatin immunoprecipitation followed by sequencing (ChIP-seq) in ATP hydrolysis mutant and in mutants that affect the level of histone H4K20 methylation and H4K16ac enrichment and depletion on the X chromosome. We have also performed Hi-C analysis to test how 3D DNA interactions mediated by condensin DC change in the catalytic and null mutant of dpy-21, a H4K20me2 demethylase that increase H4K20me1 on the X.
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