Abstract

Dosage compensation, the process by which the expression of X-linked genes are equalized between males, which have a single X chromosome and females, which have two, is essential in all heterogametic organisms. In C. elegans, dosage compensation is a complex process that is regulated by the developmental switch gene, xol-1. To better our understanding of the evolution of dosage compensation in nematodes, we use C. briggsae which has diverged from C. elegans ~15-30 million years ago, as a comparative model organism. In both species, loss of xol-1 results in a male specific lethality phenotype. We exploited this phenotype in C. briggsae and performed a classic genetic suppressor screen and identified nine suppressor mutations that are likely to represent components in the C. briggsae dosage compensation pathway.