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Genetics, Vol. 152, 999-1015, July 1999, Copyright © 1999

The Primary Sex Determination Signal of Caenorhabditis elegans

Ilil Carmia and Barbara J. Meyera
a Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley, California 94720-3204

Corresponding author: Barbara J. Meyer, Howard Hughes Medical Institute, University of California, Department of Molecular and Cell Biology, 401 Barker Hall, Berkeley, CA 94720-3204., bjmeyer{at}uclink4.berkeley.edu (E-mail)

Communicating editor: I. GREENWALD

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, promoting the male fate. Previous work has revealed at least four signal elements that repress 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.




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