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| Status |
Public on Mar 01, 2011 |
| Title |
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 |
| Organism |
Caenorhabditis elegans |
| Experiment type |
Genome binding/occupancy profiling by genome tiling array
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| Summary |
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.
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| Overall design |
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.
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| Contributor(s) |
Pferdehirt RR, Kruesi WS, Meyer BJ |
| Citation(s) |
21363964 |
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| Submission date |
Dec 03, 2010 |
| Last update date |
Mar 23, 2012 |
| Contact name |
Barbara J. Meyer |
| E-mail(s) |
bjmeyer@berkeley.edu
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| Phone |
510 643 5583
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| Organization name |
HHMI/UCB
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| Department |
MCB
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| Lab |
Meyer
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| Street address |
16 Barker Hall #3204
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| City |
Berkeley |
| State/province |
CA |
| ZIP/Postal code |
94720 |
| Country |
USA |
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| Platforms (1) |
| GPL8134 |
NimbleGen 071121_Celegans180_ChIP03_design_ID_6737 |
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| Samples (44)
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| This SubSeries is part of SuperSeries: |
| GSE25834 |
An MLL/COMPASS subunit functions in the C. elegans dosage compensation complex to target X chromosomes for transcriptional regulation of gene expression |
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| Relations |
| BioProject |
PRJNA142503 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE25833_RAW.tar |
4.0 Gb |
(http)(custom) |
TAR (of GFF, PAIR) |
| Processed data included within Sample table |
| Processed data provided as supplementary file |
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