Integrated Calendar

Genome stability requires that chromosomes be properly replicated, recombined, expressed, and segregated. These processes are controlled, in part, by an overlapping set of proteins that influence chromosome structure. This talk will focus on the shared mechanisms and protein complexes that control gene expression, chromosome segregation, and recombination.
Gene expression in multi-cellular organisms is controlled by diverse regulatory mechanisms that function over dramatically different distances, across large chromosomal territories or at individual genes. X-chromosome dosage compensation is exemplary for dissecting gene regulation over vast distances and the role of chromosome structure in that regulation. Dosage compensation ensures that males (XO or XY) and females (XX) express equal levels of gene products from their X chromosomes, despite the difference in X-chromosome dose. Although the strategies for dosage compensation differ in mammals, flies, and worms, a regulatory complex is invariably targeted to the sex chromosome of one sex to modulate transcript levels across the entire chromosome. In the round worm C. elegans, the dosage compensation complex (DCC) is targeted to both X chromosomes of hermaphrodites to repress transcript levels by about half. We showed the worm DCC resembles condensin, a protein complex required for the compaction, resolution, and segregation of mitotic and meiotic chromosomes. Not only does the DCC resemble condensin, it shares all but one subunit with two other condensin complexes in the worm, and DCC subunits also participate in other aspects of chromosome dynamics, including chromosome segregation and the regulation of crossovers between maternal and paternal chromosomes during meiosis. An important conclusion from our work is that reshuffling of the interchangeable molecular parts can create independent molecular machines with similar architectures, but with very different functions.