Figure 1

Genes analyzed in this study. (A) We analyze three components of the BRM complex in this study. In this schematic representation, Drosophila genes are labeled in blue and their human homologs are labeled in black. Shapes, sizes, and locations have no significance. Additional complex components are not shown. (B) We analyze three components of the TIP60 complex in this study. Symbols are as in (A). (C) Bap55^-/-in this study denotes the LL05955 allele, which contains a piggyBac insertion in the coding sequence (CDS) [22]. (D) brm^-/-denotes the brm²allele, an ethylmethanesulfonate (EMS) mutant that is a protein null [27]. (E) Snr1^-/- denotes the Snr1^6Callele, which is a deletion removing much of the Snr1 gene and extending into the next gene, HDAC3. HDAC3 mutants have been previously shown to have no phenotype in PNs [8]. Yet in this study we also expressed UAS-HDAC3-3xFLAG in the Snr1^6Cmutant PNs to account for any phenotypes due to HDAC3 deletion. We additionally analyzed the 01319 allele, a P-element insertion in the Snr1 coding sequence, which gave the same phenotypes as the Snr1^6Callele (data not shown). (F) dom^-/-denotes the LL05537 allele, which contains a piggyBac insertion in an intron upstream of the translational start. The piggyBac element contains splice acceptor sites and stop codons in all three coding frames [22], which likely disrupts all dom isoforms. (G) E(Pc)^-/-denotes the E(Pc)¹allele, an EMS mutant in which E(Pc)¹/+ heterozygous flies exhibit only 10 to 21% of the mRNA of wild-type flies. In principle, a null would be expected to have 50% [35]. Scale bars are provided for each panel.