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.
Highlights
Proper development requires the precise regulation of gene expression
Dosage compensation is a specialized mechanism of chromosome-wide gene regulation, by which the expression of X -linked genes are equalized between males, which have a single X chromosome and females, which have two
Standard C. elegans genetic techniques [16] were used to build the C. briggsae him-8(v188); xol-1(y430) strain used in the suppressor screen
Summary
Proper development requires the precise regulation of gene expression. In addition to individual genes being required to be expressed at the right time and place during development, chromosome-wide gene regulation events, such as dosage compensation, are required. Dosage compensation is a specialized mechanism of chromosome-wide gene regulation, by which the expression of X -linked genes are equalized between males, which have a single X chromosome and females, which have two. Dosage compensation provides us with an interesting situation in which to study evolution since numerous unrelated organisms have evolved different mechanisms to achieve this global regulation of chromosome activity. This process occurs differently in mammals (XX/XY), flies (XX/XY) and worms (XX/XO). In worms, decreasing the level of transcription of both sets of each X-linked gene in hermaphrodites relative to males equalizes X-linked gene expression between the sexes [3]
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