Abstract
Background: Condensins are multi-subunit protein complexes that are essential for chromosome condensation during mitosis and meiosis, and play key roles in transcription regulation during interphase. Metazoans contain two condensins, I and II, which perform different functions and localize to different chromosomal regions. Caenorhabditis elegans contains a third condensin, IDC, that is targeted to and represses transcription of the X chromosome for dosage compensation.Results: To understand condensin binding and function, we performed ChIP-seq analysis of C. elegans condensins in mixed developmental stage embryos, which contain predominantly interphase nuclei. Condensins bind to a subset of active promoters, tRNA genes and putative enhancers. Expression analysis in kle-2-mutant larvae suggests that the primary effect of condensin II on transcription is repression. A DNA sequence motif, GCGC, is enriched at condensin II binding sites. A sequence extension of this core motif, AGGG, creates the condensin IDC motif. In addition to differences in recruitment that result in X-enrichment of condensin IDC and condensin II binding to all chromosomes, we provide evidence for a shared recruitment mechanism, as condensin IDC recruiter SDC-2 also recruits condensin II to the condensin IDC recruitment sites on the X. In addition, we found that condensin sites overlap extensively with the cohesin loader SCC-2, and that SDC-2 also recruits SCC-2 to the condensin IDC recruitment sites.Conclusions: Our results provide the first genome-wide view of metazoan condensin II binding in interphase, define putative recruitment motifs, and illustrate shared loading mechanisms for condensin IDC and condensin II.
| Original language | English (US) |
|---|---|
| Article number | R112 |
| Journal | Genome biology |
| Volume | 14 |
| Issue number | 10 |
| DOIs | |
| State | Published - Nov 14 2013 |
| Externally published | Yes |
Bibliographical note
Funding Information:We thank Andreas Hochwagen and Kirsten Hagstrom for comments on the manuscript, Kirsten Hagstrom for anti-HCP-6, anti-SMC-4 and anti-DPY-28, and Arshad Desai for anti-SMC-4 antibody. We thank Niyati Parikh, Uchita Patel and Brent Chen for help with various aspects of the experiments, and the UNC and NYU-CGSB High Throughput Sequencing Facilities for sequencing and raw data processing. This research was supported in part by modENCODE grant U01 HG0044270 to Jason Lieb and March of Dimes Foundation grant 5-FY12-118 to Sevinc Ercan. Some strains were provided by the CGC, which is funded by NIH Office of Research Infrastructure Programs (P40 OD010440).