Caenorhabditis elegans
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PROVIDER: PRJNA209991 | ENA |
REPOSITORIES: ENA
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Project description:The essential process of dosage compensation equalizes X-chromosome gene expression between C. elegans XO males and XX hermaphrodites through a dosage compensation complex (DCC) that resembles condensin. The DCC binds to both X chromosomes of hermaphrodites to repress transcription by half. Here we show that post-translational modification by the SUMO conjugation pathway is essential for sex-specific assembly of the DCC onto X. Depletion of the SUMO peptide in vivo severely disrupts binding of particular DCC subunits and causes changes in X-linked gene expression similar to those caused by disrupting genes encoding DCC subunits. Three DCC subunits are themselves SUMOylated, and depletion of SUMO preferentially reduces their binding to X, suggesting that SUMOylation of DCC subunits is essential for robust association with X. DCC SUMOylation is triggered by the signal that initiates DCC assembly onto X. The initial step of assembly--binding of X-targeting factors to recruitment sites on X (rex sites)--is independent of SUMOylation, but robust binding of the complete complex requires SUMOylation. SUMOylated DCC subunits are enriched at rex sites, and SUMOylation enhances interactions between X-targeting factors and condensin subunits that facilitate DCC binding beyond the low level achieved without SUMOylation. DCC subunits also participate in condensin complexes essential for chromosome segregation, but their SUMOylation occurs only in the context of the DCC. Our results reinforce a newly emerging theme in which multiple proteins of a complex are SUMOylated in response to a specific stimulus, leading to accelerated complex formation and enhanced function. ChIP-chip experiments using antibodies against DPY-27, SDC-3, DPY-30, DPY-26, DPY-28 and FLAG-tagged SDC-2 in wild-type and smo-1 RNAi treated mixed embryos, with IGG controls. Also, sequential ChIP-chip experiments: (1) ChIP using FLAG antibodies to determine the genome-wide binding sites for SUMOylated proteins, (2) ChIP using FLAG antibodies followed by re-ChIP of eluted protein-chromatin complexes with DPY-27 antibodies to determine genome-wide binding sites for SUMOylated DPY-27 (referred to as DPY-27 re-ChIP experiments), (3) ChIP using FLAG antibodies followed by re-ChIP of eluted protein-chromatin with IGG antibodies to determine background binding (referred to as IGG re-ChIP experiments, and (4) ChIP using DPY-27 antibodies as a control to assess the efficiency of DPY-27 binding and detection in control vs. FLAG-tagged strains.
2013-08-31 | E-GEOD-48413 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE25831: Fed L1 larvae total RNA levels by microarray GSE25833: Examination of DPY-30, DPY-27, SDC-3, DPY-26, MIX-1, SMC-4, ASH-2, RNA Polymerase II binding in wild type embryos, DCC mutant embryos, and wild type fed L1 larvae GSE25877: Comparison of DPY-27 binding in embryos and fed L1 larvae Refer to individual Series
2011-03-01 | E-GEOD-25834 | biostudies-arrayexpress
Project description:Examination of DPY-30, DPY-27, SDC-3, DPY-26, MIX-1, SMC-4, ASH-2, RNA Polymerase II binding in wild type and DCC mutant embryos
| PRJNA142503 | ENA
Project description:ChIP-seq for the SDC-2 and DPY-27 subunits of the dosage compensation complex in C. briggsae
2023-02-15 | GSE214714 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE14649: DCC binding and function (Expression Analysis) GSE14650: DCC binding and function (ChIP-chip: SDC-3, MIX-1, DPY-27, Mock) GSE14651: DCC binding and function (ChIP-chip: DPY-27) GSE14652: DCC binding and function (ChIP-chip: SDC-2) GSE14653: DCC binding and function (ChIP-chip: SDC-3, DPY-27, Mock) Refer to individual Series
2010-05-22 | E-GEOD-14640 | biostudies-arrayexpress
Project description:Here we exploit the essential process of X-chromosome dosage compensation to elucidate basic mechanisms that control the assembly, genome-wide binding, and function of gene regulatory complexes that act over large chromosomal territories. We demonstrate that a subunit of C. elegans MLL/COMPASS, a gene-activation complex, acts within the dosage compensation complex (DCC), a condensin complex, to target the DCC to both X chromosomes of hermaphrodites and thereby reduce chromosome-wide gene expression. The DCC binds to two categories of sites on X: rex sites that recruit the DCC in an autonomous, sequence- dependent manner, and dox sites that reside primarily in promoters of expressed genes and bind the DCC robustly only when attached to X. We find that DCC mutants that abolish rex-site binding do not eliminate dox-site binding, but instead reduce it to the level observed at autosomal binding sites in wild-type animals. Changes in DCC binding to these non-rex sites occur throughout development and correlate with transcriptional activity of adjacent genes. Moreover, autosomal DCC binding is enhanced by rex-site binding in cis in X-autosome fusion chromosomes. Thus, dox and autosomal sites exhibit similar binding properties. Our data support a model for DCC binding in which low-level DCC binding at dox and autosomal sites is dictated by intrinsic properties correlated with high transcriptional activity. Sex-specific DCC recruitment to rex sites then greatly elevates DCC binding to dox sites in cis, which lack intrinsically high DCC affinity on their own. We also show here that the C. elegans DCC achieves dosage compensation through its effects on transcription. ChIP-chip experiments using antibodies against DPY-27, SDC-3, DPY-30, DPY-26, MIX-1, SMC-4, ASH-2 in wild-type embryos. ChIP-chip experiments using antibodies against SDC-3, DPY-27, DPY-30, ASH-2, and IgG in different DCC mutants. ChIP-chip experiments using antibodies against RNA Pol II (hypophosphorylated and S2 and S5) in wild type and sdc-2 partial loss of function mutants.
2011-03-01 | E-GEOD-25833 | biostudies-arrayexpress
Project description:In C. elegans, a condensin-like protein complex associates specifically with both X chromosomes of XX animals to execute dosage compensation. Dosage Compensation Complex (DCC) reduces the level of transcripts arising from each of the two X chromosomes. Recruitment to X is specified in part by discrete DNA sequence motifs, but following recruitment, the DCC is targeted to the promoters of individual active genes by an unknown mechanism. Here, we investigated three outstanding questions regarding the molecular mechanism of DCC recruitment and spreading along X. By examining the genome-wide binding patterns of several DCC subunits in different stages of C. elegans development, and in strains harboring X:Autosome chromosomal fusions, we provide evidence that: (1) DCC binding is dynamically specified according to gene activity during development (2) The condensin-like subunits of the DCC spread from recruitment sites to active promoters more readily than the non-conserved SDC subunits, which are involved in initial X-targeting and (3) the mechanism of DCC spreading is independent of X-chromosome DNA sequence, and will proceed onto any active promoter near a recruitment site. Our results contribute to understanding how chromatin complexes can be targeted to achieve domain-scale transcriptional regulation during development. ChIP-chip analysis of SDC-2, DPY-26 and MIX-1 were done in C elegans N2 embryos. DPY-27 and RNA Polymerase II ChIP-chip were performed in N2 L4s. DPY-27 ChIP-chip in X-autosome fusions were done, X chromosome fused to either V (YPT47), II (YPT41) or I (11dh). RNA abundance analysis in N2, YPT41 and YPT47 embryos are included.
2009-11-15 | E-GEOD-16621 | biostudies-arrayexpress
Project description:Caenorhabditis briggsae SDC-2 and DPY-27 ChIP-seq
| PRJNA886730 | ENA
Project description:DCC binding and function (ChIP-chip: SDC-3, DPY-27, Mock)
| PRJNA114419 | ENA
Project description:DCC binding and function (ChIP-chip: SDC-3, MIX-1, DPY-27, Mock)
| PRJNA114439 | ENA