Caenorhabditis elegans Dosage Compensation: Insights into Condensin-Mediated Gene Regulation

Trends

The core of the Caenorhabditis elegans DCC is a specialized condensin that differs from the canonical condensin I by a single SMC-4 variant, DPY-27 [21].

Genome-wide analyses of DCC and canonical condensin binding in C. elegans indicate conservation in the genomic localization of different types of condensin complexes [22].

X recognition by DCC occurs at a limited number of strong recruitment sites, which contain multiple copies of a 12-bp sequence motif and overlap with HOT sites 35, 38, 39.

Long-distance cooperation between recruitment sites on the X establish and reinforce robust DCC binding [39].

Following recruitment, DCC spreads linearly across megabase distances flanked by TAD boundaries 37, 39.

DCC represses transcription by reducing RNA Pol II binding to X-chromosome promoters 33, 77, 78, 79, 80.

DCC regulates compaction, nuclear localization 86, 89, TAD organization [57], and levels of H4K20me1 and H4K16ac on the X chromosomes 31, 77, 92, 93.

Recent work demonstrating the role of chromosome organization in transcriptional regulation has sparked substantial interest in the molecular mechanisms that control chromosome structure. Condensin, an evolutionarily conserved multisubunit protein complex, is essential for chromosome condensation during cell division and functions in regulating gene expression during interphase. In Caenorhabditis elegans, a specialized condensin forms the core of the dosage compensation complex (DCC), which specifically binds to and represses transcription from the hermaphrodite X chromosomes. DCC serves as a clear paradigm for addressing how condensins target large chromosomal domains and how they function to regulate chromosome structure and transcription. Here, we discuss recent research on C. elegans DCC in the context of canonical condensin mechanisms as have been studied in various organisms.