The autosomal signal in Caenorhabditis elegans sex determination

In the nematode C. elegans, the X:A ratio acts as the primary signal to determine sex and to establish dosage compensation. In XX animals, two doses of X-signal elements (XSEs) repress the master switch gene xol-1 (XO-lethal 1). As a consequence, the hermaphrodite fate is chosen and dosage compensation complexes bind to and repress transcription of both X chromosomes. In XO animals, a single dose of XSEs is not sufficient to repress xol-1. High levels of xol-1 cause the male fate to be chosen and prevent hermaphrodite dosage compensation complexes from binding to the single X chromosome.;XSEs promote the hermaphrodite fate by repressing xol-1. SEX-1 and CEH-39 repress xol-1 transcription directly by binding to its promoter. fox-1 encodes an RNA-binding protein that represses xol-1 post-transcriptionally by preventing the proper splicing of xol-1 pre-mRNA.;This work describes the autosomal component of the X:A ratio that determines sex in C. elegans. The autosomal component is analogous to the X component and is made up of discrete autosomal genes termed autosomal signal elements (ASEs) that oppose XSEs. Chapter 2 describes the identification, genetic characterization and molecular analysis of sea-1, the first ASE in C. elegans. Chapter 3 describes the identification of SEA-1 binding sites in the xol-1 promoter and their importance in activating xol-1 transcription. These chapters demonstrate that in worms, the autosomal component of the X:A ratio consists, at least in part, of a discrete gene whose product directly activates transcription of the master switch gene. This direct antagonism between the ASEs and XSEs translates a twofold difference in X chromosome dose into either the male or hermaphrodite sexual fate.