In animals whose sex is determined by sex chromosomes, there has to be some mechanism by which the amount of X chromosome gene expression is equalized for males and females. This mechanism is known as dosage compensation. Previously we discussed mammalian X-chromosome inactivation, whereby one of the X chromosomes is inactivated so that the transcription product level is the same in both XX cells and XY cells.
In the worm Caenorhabditis elegans, dosage compensation occurs by lowering the transcription rates of both X chromosomes so that product levels are the same as those of XO individuals.
In Drosophila, the female X chromosome is not suppressed; rather, the male’s single X chromosome is hyperactivated. This “hypertranscription” is accomplished at the level of translation and is mediated by the Sxl protein. Sxl (which is made by the female cells; see earlier discussion) binds to the 5ʹ leader sequence and the 3ʹ untranslated regions of the msl2 message. The bound Sxl inhibits the attachment of msl2 mRNA to the ribosome and prevents the ribosome from getting to the mRNA coding region (Beckman et al. 2005). The result is that female cells do not produce Msl2 protein (see textbook Figure 6.14), but Msl2 is made in male cells, in which Sxl is not present. Msl2 is part of a protein-mRNA complex that targets the X chromosome and loosens its chromatin structure by acetylating histone 4 (see textbook Figure 3.5). In this way, transcription factors gain access to the X chromosome at a much higher frequency in males than in females—hence, “hypertranscription.”
Beckman, K., M. Grskovic, F. Gebauer and M. W. Hentze. 2005. A dual inhibitory mechanism restricts Msl-2 mRNA translation for dosage compensation in Drosophila. Cell 122: 529–540.