An X chromosome counting process determines sex in Caenorhabditis elegans. The dose of X chromosomes is translated into sexual fate by a set of X-linked genes that together control the activity of the sex-determination and dosage-compensation switch gene,
xol-1. The double dose of X elements in XX animals represses
xol-1 expression, promoting the hermaphrodite fate, while the single dose of X elements in XO animals permits high
xol-1 expression at two levels, transcriptional and post-transcriptional. The two molecularly characterized elements include an RNA binding protein and a nuclear hormone receptor homolog. Here we explore the roles of the two mechanisms of
xol-1 repression and further investigate how the combined dose of X signal elements ensures correct, sex-specific expression of
xol-1. By studying the effects of increases and decreases in X signal element dose on male and hermaphrodite fate, we demonstrate that signal elements repress
xol-1 cumulatively, such that full repression of
xol-1 in XX animals results from the combined effect of individual elements. Complete transformation from the hermaphrodite to the male fate requires a decrease in the dose of all four elements, from two copies to one. We show that both mechanisms of
xol-1 repression are essential and act synergistically to keep
xol-1 levels low in XX animals. However, increasing repression by one mechanism can compensate for loss of the other, demonstrating that each mechanism can exert significant
xol-1 repression on its own. Finally, we present evidence suggesting that
xol-1 activity can be set at intermediate levels in response to an intermediate X signal.