in such organisms for the Y chromosome to be necessary for male fertility, but not for it to play an explicit role in sex determination. In Drosophila, for example, the sex lethal (SXL) gene acts as a key regulator of sexual differentiation and maturation in somatic tissue; in XX animals, SXL is activated to repress increased transcription, while in XY animals SXL is inactive and allows male development to proceed via increased transcription of the single X. Several binding sites exist on the Drosophila X chromosome for the dosage compensation complex (DCC), a ribonucleoprotein complex; these binding sites have varying levels of affinity, presumably for varying expression of specific genes. The Male Specific Lethal complex, composed of protein and RNA binds and selectively modifies hundreds of X-linked genes, increasing their transcription to levels comparable to female D. melanogaster. In organisms that use this method of dosage compensation, the presence of one or more X chromosomes must be detected early on in development, as failure to initiate the appropriate dosage compensation mechanisms is lethal. Male specific lethal proteins (MSLs) are a family of four proteins that bind to the X chromosome exclusively in males. The name “MSL” is used because mutations in these genes cause inability to effectively upregulate X-linked genes appropriately, and are thus lethal to males only and not their female counterparts. SXL regulates pre-messenger RNA in males to differentially splice MSLs and result in the appropriate increase in X chromosome transcription observed in male Drosophila. The immediate target of SXL is male specific lethal-2 (MSL-2). Current dogma suggests that the binding of MSL-2 at multiple sites along the SXL gene in females prevents proper MSL-2 translation, and thus, as previously stated, represses the possibility for X-linked genetic upregulation in females. However, all other transcription factors in the MSL family—maleless, MSL-1, and MSL-3—are able to act when SXL is not expressed, as in the case in males. These factors act to increase male X chromosome transcriptional activity. Histone acetylation and the consequent upregulation of X-linked genes in males is dictated by the MSL complex. Specifically, special roX non-coding RNAs on the MSL complexes facilitate binding to the single male X chromosome, and dictate acetylation of specific loci along the X chromosome as well as the formation of euchromatin. Though these RNAs bind at specific sites along the male X chromosome, their effects spread along the length of the chromosome