SRA

Dosage compensation in D. melanogaster males is achieved via targeting of the MSL complex to X chromosomal genes. This is proposed to involve initial sequence-specific recognition of the X at ~150-300 chromatin entry sites, and subsequent spreading to nearby active genes. Here we test a model in which the spreading step requires transcription and is sequence-independent. We ask whether, in the native context of the X chromosome, MSL complex will target genes of autosomal origin. We find that MSL complex does bind such genes, but only if transcriptionally active. Targeting is accompanied by acetylation of the histone H4K16 residue and two-fold transcriptional up-regulation. We conclude that the presence of a long-sought specific DNA sequence within X-linked genes is not obligatory for MSL complex binding. Instead, physical linkage and transcription play the pivotal roles in the identification of MSL targets irrespective of their origin and DNA sequence. Keywords: Epigenetics Overall design: ChIP-seq measurements of MSL complex binding and input control. Chromatin was prepared from third instar male larvae of a genotype y w TrojanElephant; MSL3-TAP; msl3. TrojanElephant is a mini-white- and yellow-marked transposition of genomic region spanning 65 kb from cg13773 to snRNP70K. MSL3-TAP is a mini-white-marked TAP-tagged genomic msl3 transgene. IgG beads were used for pull-down.