Sexual Dimorphism of Body Size Is Controlled by Dosage of the -Chromosomal Gene and by the Sex-Determining Gene in .

females are larger than males. In this article, we describe how -chromosome dosage drives sexual dimorphism of body size through two means: first, through unbalanced expression of a key -linked growth-regulating gene, and second, through female-specific activation of the sex-determination pathway. -chromosome dosage determines phenotypic sex by regulating the genes of the sex-determining pathway. In the presence of two sets of -chromosome signal elements (XSEs), () is activated in female () but not male () animals. Sxl activates (), a gene that encodes a splicing factor essential for female-specific development. It has previously been shown that null mutations in the gene result in only a partial reduction of body size of animals, which shows that other factors must contribute to size determination. We tested whether dosage directly affects animal size by analyzing males with duplications of -chromosomal segments. Upon tiling across the chromosome, we found four duplications that increase male size by >9%. Within these, we identified several genes that promote growth as a result of duplication. Only one of these, , was found not to be dosage compensated. Together, our results indicate that both dosage and expression play crucial roles in determining sex-specific size in larvae and adult tissue. Since also acts as an XSE that contributes to activation in early development, a double dose of in females serves at least twice in development to promote sexual size dimorphism.