Expression of X-linked genes (one X in males, two X's in females) is equalized by hypertranscription of the male X.

Salivary gland polytene chromosomes from a male third instar larvae
(A: DNA stain, B: MSL-1 stain on the X chromosome)

Current model for the regulation of msl-mediated dosage compensation.
In females, where the X to autosome ratio is one, the Sxl gene is turned on and it functions to repress the translation of msl-2. Both msl-2 UTRs are important for preventing MSL-2 protein expression in females. SXL binding sites in the 3' UTR are proposed to be a target for translational repression by SXL. SXL also functions in females to prevent the removal of a small intron in the 5'UTR. In the absence of MSL-2 protein, the other MSLs are unable to associate with the X chromosomes, H4Ac16 does not accumulate and the female X's are not hypertranscribed. In males, where the X to autosome ratio is 0.5, Sxl is off. In the absence of SXL protein, the small intron in the msl-2 5' UTR is removed, MSL-2 protein is expressed and the full complement of MSLs associates with the male X (see Fig. A + B). This results in the recruitment of H4Ac16, the alteration of chromatin structure and hypertranscription. (Genes = rectangles. Transcripts = rounded rectangles. The UTRs of MSL-2 = thinner rounded rectangles. The retained intron is shaded in female msl-2 RNAs. The potential SXL binding sites in the 3' UTR = black vertical lines. Proteins = ovals.)