Final answer:
Having two copies of the X-chromosome gene, Sex lethal (Sxl), initiates the female sex-determining pathway through gene splicing mechanisms and X-chromosome inactivation. Sxl regulates splicing of the tra gene, affecting the expression of genes leading to female characteristics. The process of X inactivation balances gene dosage in females, with one X chromosome forming a Barr body.
Step-by-step explanation:
Having two copies of the X-chromosome gene, Sex lethal (Sxl), initiates the female sex-determining pathway by means of gene regulatory mechanisms involving gene splicing and X-chromosome inactivation. In the fruit fly Drosophila melanogaster, the Sxl gene is expressed only in the presence of two X chromosomes, which is the case for females. The product of Sxl acts as a splicing repressor, modulating the splicing of another gene called transformer (tra). In females, Sxl causes tra to be spliced into a female form, leading to the expression of other genes, such as doublesex (dsx) and fruitless (fru), which result in female sexual characteristics. In the absence of the Sxl product, as in males, tra undergoes default splicing leading to male characteristics.
In mammalian females, the process of X inactivation balances the gene dosage between males and females. During embryonic development, one of the two X chromosomes condenses into a Barr body, becoming inactive, which prevents the overexpression of X-linked genes in females. This process of inactivation is random for each cell and is passed down to descendant cells, maintaining the same inactivated X chromosome, balancing the double genetic dose of the X chromosome. This epigenetic mechanism has observable consequences in conditions such as tortoiseshell cats, where color variegation reveals which X chromosome is inactivated in different areas of the skin.