<i>Guy1</i>, a Y-linked embryonic signal, regulates dosage compensation in <i>Anopheles stephensi</i> by increasing X gene expression.

Abstract

We previously showed that <i>Guy1</i>, a primary signal expressed from the Y chromosome, is a strong candidate for a male-determining factor that confers female-specific lethality in <i>Anopheles stephensi</i> (Criscione et al., 2016). Here, we present evidence that <i>Guy1</i> increases X gene expression in <i>Guy1</i>-transgenic females from two independent lines, providing a mechanism underlying the <i>Guy1</i>-conferred female lethality. The median level gene expression (MGE) of X-linked genes is significantly higher than autosomal genes in <i>Guy1</i>-transgenic females while there is no significant difference in MGE between X and autosomal genes in wild-type females. Furthermore, <i>Guy1</i> significantly upregulates at least 40% of the 996 genes across the X chromosome in transgenic females. <i>Guy1</i>-conferred female-specific lethality is remarkably stable and completely penetrant. These findings indicate that <i>Guy1</i> regulates dosage compensation in <i>An. stephensi</i> and components of dosage compensation may be explored to develop novel strategies to control mosquito-borne diseases.