Genetic interactions of histone acetyl-transferase enzymes encoding genesGcn5andMofwithhsrωlncRNA gene

The hsrω 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 hsrω 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 hsrω . 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 hsrω , but not by down regulation through hsrω-RNAi . Likewise, eye phenotypes following ey-GAL4 driven down-regulation of Gcn5 or Mof were also partially suppressed by over-expression of hsrω. Act-GAL4 driven global over-expression of hsrω 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 hsrω 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 hsrω 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 hsrω are known to have important roles.