Reports

first (MOF) within the male-specific lethal (MSL) complex mediates global hyper-acetylation of X-linked chromatin at H4K16 (1, 2). The mark is thought to mediate a two-fold upregulation of X-linked tran-scription by promoting the formation of an accessible chromatin struc-ture (3–6). However, the mechanism of this activation has remained elusive. It has been proposed that dosage compensation occurs by en-hanced transcription elongation through male X-linked genes (7, 8), although direct support for this claim is limited. The study of dosage compensation has been complicated by the rela-tively small magnitude of the two-fold increase in transcription rate and by the widespread use of aneuploid male cell-lines as the model system. A shortcoming has been the lack of direct comparison of Pol II-occupancies between male and female flies. Without reference meas-urements in females, it is not possible to distinguish sex-specific from gene-specific effects. This is essential in order to draw unambiguou