Abstract

The hsr{omega} lncRNAs are known to interact with the Iswi chromatin remodeler while Iswi is known to interact with Gcn5, a general histone acetyl transferase, and Mof, a male-specific HAT essential for H4K16 acetylation and consequent hyperactivity of the single X-chromosome in male Drosophila. We show here that hsr{omega} genetically interacts with Gcn5 as well as Mof, but unlike the suppression of phenotypes due to down-regulation or absence of Iswi, those following down-regulation of Gcn5 or Mof are suppressed by over-expression of hsr{omega}. General lethality caused by Act-GAL4 driven global expression of Gcn5-RNAi and the male-specific lethality following Mof-RNAi transgene expression were partially suppressed by over-expression of hsr{omega}, but not by down regulation through hsr{omega}-RNAi. Likewise, eye phenotypes following ey-GAL4 driven down-regulation of Gcn5 or Mof were also partially suppressed by over-expression of hsr{omega}. Act-GAL4 driven global over-expression of hsr{omega} along with Gcn5-RNAi transgene substantially restored levels of Gcn5 RNA as well as protein that were reduced by Gcn5-RNAi. Mof-RNAi transgene expression reduced Megator and Msl-2 levels and their nuclear distribution patterns; over-expression of hsr{omega} along with Mof-RNAi substantially restored Megator levels and its distribution at the nuclear rim and in nucleoplasmic speckles and at the same time restored the male X-chromosome specific localization of Msl-2. Earlier reported antagonistic interactions of Mof with Iswi and interaction of hsr{omega} transcripts with Megator appear to underlie the suppression of Gcn5 and Mof phenotypes by over-expression of the lncRNAs. Present results add the dosage compensation pathway to the list of diverse pathways in which the multiple lncRNAs produced by the hsr{omega} are known to have important roles.