Analysis of SDC-2, DPY-26, MIX-1, DPY-27 and RNA Polymerase II ChIP-chip and RNA abundance in C. elegans

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. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf 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.