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Figure 1. The X:A sex

determining signal. (Top),

X-chromosome dose is assessed

with high fidelity relative to the

ploidy (the sets of autosomes),

resulting in embryos with ratios of

0.5 or 0.67 developing into fertile

males, and those with ratios of 0.75

or 1.0 into fertile hermaphrodites.

(Bottom), Genetic properties of

XSEs and ASEs. Genes encoded on

X called X-signal elements (XSEs)

repress the master

sex-determining gene xol-1, while

genes on autosomes called

autosomal signal element (ASEs)

activate it. The double dose of XSEs

in 2X:2A embryos counteracts the

double dose of ASEs to repress

xol-l, thereby promoting

hermaphrodite development and

DCC assembly onto X. In contrast,

the double dose of ASEs in 1X:2A

embryos counteracts the single

dose of XSEs to activate xol-1 and

promote the male fate. Mutations

that knock out XSEs in 2X:2A

embryos activate xol-1, causing the

masculinization and death of

embryos from the disruption of

dosage compensation and the

consequent elevation in X-linked

gene expression. Reducing the

dose of ASEs in XSE-deficient 2X:2A

animals restores the X:A signal,

thereby repressing xol-1 and

restoring viability.

Figure 1. The X:A sex determining signal. (Top), X-chromosome dose is

assessed with high fidelity relative to the ploidy (the sets of autosomes), resulting in

embryos with ratios of 0.5 or 0.67 developing into fertile males, and those with

ratios of 0.75 or 1.0 into fertile hermaphrodites. (Bottom), Genetic properties of

XSEs and ASEs. Genes encoded on X called X-signal elements (XSEs) repress the

master sex-determining gene xol-1, while genes on autosomes called autosomal

signal element (ASEs) activate it. The double dose of XSEs in 2X:2A embryos

counteracts the double dose of ASEs to repress xol-l, thereby promoting

hermaphrodite development and DCC assembly onto X. In contrast, the double

dose of ASEs in 1X:2A embryos counteracts the single dose of XSEs to activate xol-1

and promote the male fate. Mutations that knock out XSEs in 2X:2A embryos

activate xol-1, causing the masculinization and death of embryos from the

disruption of dosage compensation and the consequent elevation in X-linked gene

expression. Reducing the dose of ASEs in XSE-deficient 2X:2A animals restores the

X:A signal, thereby repressing xol-1 and restoring viability.

Figure 1. The X:A sex determining signal. (Top), X-chromosome dose is assessed with high fidelity relative to the

ploidy (the sets of autosomes), resulting in embryos with ratios of 0.5 or 0.67 developing into fertile males, and those

with ratios of 0.75 or 1.0 into fertile hermaphrodites. (Bottom), Genetic properties of XSEs and ASEs. Genes encoded

on X called X-signal elements (XSEs) repress the master sex-determining gene xol-1, while genes on autosomes called

autosomal signal element (ASEs) activate it. The double dose of XSEs in 2X:2A embryos counteracts the double dose

of ASEs to repress xol-l, thereby promoting hermaphrodite development and DCC assembly onto X. In contrast, the

double dose of ASEs in 1X:2A embryos counteracts the single dose of XSEs to activate xol-1 and promote the male

fate. Mutations that knock out XSEs in 2X:2A embryos activate xol-1, causing the masculinization and death of

embryos from the disruption of dosage compensation and the consequent elevation in X-linked gene expression.

Reducing the dose of ASEs in XSE-deficient 2X:2A animals restores the X:A signal, thereby repressing xol-1 and

restoring viability.