Originally published as Genetics Published Articles Ahead of Print on October 18, 2007.

Genetics, Vol. 177, 1639-1654, November 2007, Copyright © 2007
doi:10.1534/genetics.107.078071

Revisiting the X:A Signal That Specifies Caenorhabditis elegans Sexual Fate

Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley, California 94720-3204

1 Corresponding author: Department of Molecular and Cell Biology, Howard Hughes Medical Institute, 16 Barker Hall, MC 3204, University of California, Berkeley, CA 94720-3204.
E-mail: bjmeyer{at}berkeley.edu

In Caenorhabditis elegans, sex is determined by the opposing actions of X-signal elements (XSEs) and autosomal signal elements (ASEs), which communicate the ratio of X chromosomes to sets of autosomes (X:A signal). This study delves more deeply into the mechanism by which XSEs transmit X chromosome dose. We determined the relative contributions of individual XSEs to the X:A signal and showed the order of XSE strength to be sex-1 > sex-2 > fox-1 > ceh-39 ≥ region 1 XSE. sex-1 exerts a more potent influence on sex determination and dosage compensation than any other XSE by functioning in two separate capacities in the pathway: sex-1 acts upstream as an XSE to repress xol-1 and downstream as an activator of hermaphrodite development and dosage compensation. Furthermore, the process of dosage compensation affects expression of the very XSEs that control it; XSEs become fully dosage compensated once sex is determined. The X:A signal is then equivalent between XO and XX animals, causing sexual differentiation to be controlled by genes downstream of xol-1 in the sex-determination pathway. Prior to the onset of dosage compensation, the difference in XSE expression between XX and XO embryos appears to be greater than twofold, making X chromosome counting a robust process.




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J. M. Gladden and B. J. Meyer
A ONECUT Homeodomain Protein Communicates X Chromosome Dose to Specify Caenorhabditis elegans Sexual Fate by Repressing a Sex Switch Gene
Genetics, November 1, 2007; 177(3): 1621 - 1637.
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