Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1037740 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26782189_1.fastq.gz | Fastqsanger.gz | |||
| SRR26782189_2.fastq.gz | Fastqsanger.gz | |||
| SRR26782190_1.fastq.gz | Fastqsanger.gz | |||
| SRR26782190_2.fastq.gz | Fastqsanger.gz | |||
| SRR26782191_1.fastq.gz | Fastqsanger.gz |
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Project description:Genomic analysis of the entomopathogenic nematode Steinernema hermaphroditum
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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: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:Animals change developmental fates in response to external cues. In the nematode Caenorhabditis elegans, unfavorable environmental conditions induce a state of diapause known as dauer by inhibiting the conserved DAF-2 insulin-like signaling (ILS) pathway through incompletely understood mechanisms. We previously established a role for the C. elegans dosage compensation protein DPY-21 in the control of dauer arrest and DAF-2 ILS. Here we show that dosage compensation acts through the histone H4 lysine 20 methyltransferase SET-4 to promote dauer arrest in part by repressing the X-linked ins-9 gene, which encodes a new agonist insulin-like peptide (ILP) expressed specifically in the paired ASI sensory neurons that are required for dauer bypass. ins-9 repression in dauer-constitutive mutants requires DPY-21, SET-4, and the FoxO transcription factor DAF-16, which is the main target of DAF-2 ILS. In contrast, autosomal genes encoding major agonist ILPs that promote reproductive development are not repressed by DPY-21, SET-4, or DAF-16/FoxO. Our results implicate the dosage compensation machinery as a sensory rheostat that reinforces developmental fates in response to environmental cues by modulating autocrine and paracrine DAF-2 ILS.
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Project description:Mechanisms of X chromosome dosage compensation have been studied in model organisms with distinct sex chromosome ancestry. However, the diversity of mechanisms as a function of sex chromosome evolution is largely unknown. Here, we anchor ourselves to the nematode Caenorhabditis elegans, where dosage compensation is accomplished by an X chromosome specific condensin that belongs to the family of structural maintenance of chromosomes (SMC) complexes. By combining a phylogenetic analyses of the C. elegans dosage compensation complex with a comparative analysis of its epigenetic signatures, such as X-specific topologically associating domains (TADs) and enrichment of H4K20me1, we show that the condensin-mediated mechanism evolved recently in the lineage leading to Caenorhabditis following an SMC-4 duplication. Unexpectedly, we found an independent duplication of SMC-4 in Pristionchus pacificus along with X-specific TADs and H4K20me1 enrichment, which suggests that condensin-mediated dosage compensation evolved more than once in nematodes. Differential expression analysis between sexes in several nematode species indicates that dosage compensation itself precedes the evolution of X-specific condensins. In Rhabditina, X-specific condensins may have evolved in the presence of an existing mechanism linked to H4K20 methylation as Oscheius tipulae X chromosomes are enriched for H4K20me1 without SMC-4 duplication or TADs. In contrast, Steinernema hermaphroditum lacks H4K20me1 enrichment, SMC-4 duplication, and TADs. Together, our results indicate that dosage compensation mechanisms continue to evolve in species with shared X chromosome ancestry, and SMC complexes may have been co-opted at least twice in nematodes, suggesting that the process of evolving chromosome wide gene regulatory mechanisms are constrained.
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Project description:We identified the DNA binding sites of DPY-27 in C. elegans. DPY-27 was C-terminally tagged with GFP and the expression pattern was examined through fluorescent microscopy. The binding sites were determined using chromatin immunoprecipitation with anti-GFP antibody followed by illumina high-throughput sequencing (ChIP-seq). For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Identification of DPY-27 binding sites at embryonic stage
2009-04-03 | E-GEOD-15501 | biostudies-arrayexpress
Project description:We identified the DNA binding sites of DPY-27 in C. elegans. DPY-27 was C-terminally tagged with GFP and the expression pattern was examined through fluorescent microscopy. The binding sites were determined using chromatin immunoprecipitation with anti-GFP antibody followed by illumina high-throughput sequencing (ChIP-seq). For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
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