Artyom A. Alekseyenko، نويسنده , , Shouyong Peng، نويسنده , , Erica Larschan، نويسنده , , Andrey A. Gorchakov، نويسنده , , Ok-Kyung Lee، نويسنده , , Peter Kharchenko، نويسنده , , Sean D. McGrath، نويسنده , , Charlotte I. Wang، نويسنده , , Elaine R. Mardis، نويسنده , , Peter J. Park، نويسنده , , Mitzi I. Kuroda، نويسنده ,
The Drosophila MSL complex associates with active genes specifically on the male X chromosome to acetylate histone H4 at lysine 16 and increase expression approximately 2-fold. To date, no DNA sequence has been discovered to explain the specificity of MSL binding. We hypothesized that sequence-specific targeting occurs at “chromatin entry sites,” but the majority of sites are sequence independent. Here we characterize 150 potential entry sites by ChIP-chip and ChIP-seq and discover a GA-rich MSL recognition element (MRE). The motif is only slightly enriched on the X chromosome (∼2-fold), but this is doubled when considering its preferential location within or 3′ to active genes (>4-fold enrichment). When inserted on an autosome, a newly identified site can direct local MSL spreading to flanking active genes. These results provide strong evidence for both sequence-dependent and -independent steps in MSL targeting of dosage compensation to the male X chromosome.