Fig. 2. Cartoon of the pygo locus and mutant alleles and pygo expression profile. (A) The pygo locus with flanking genes rough deal (rod) and -cop. The location and orientation of the EP(3)1076 transposon is also shown. Besides the Gal4-dependent dominant phenotypes seen with EP(3)1076, the transposon also causes a Gal4-independent recessive phenotype (referred to as pygo^EP). (B) Depiction of two additional pygo loss-of-function alleles created by imprecise excision of EP(3)1076. pygo¹⁰ contains half of the transposon and removes the splice acceptor site in the 5' UTR intron of the pygo gene, and the first 295 residues of the Pygo ORF. It does not affect rod (see Results). The pygo⁹ mutation extends further upstream of pygo, and inactivates rod as well. In situ hybridization of embryos (C-F) and wing imaginal discs (G,H) with a probe for pygo. Preblastoderm wild-type embryo (C) shows high levels of staining that are absent in pygo¹⁰ germline clones (D). At stage 10, wild-type embryos (E) show ubiquitous staining at a much lower level than in C (the preparation was allowed to develop much longer). Stage 10 embryos maternally and zygotically mutant for the pygo¹⁰ allele (F; identified by their altered morphology) presumably indicate the level of background staining under these conditions. Late third instar wing imaginal discs show low levels of ubiquitous signal (G), while discs containing random clones of Gal4-expressing cells (via an actin promoter) in a EP(3)1076 background show patches of cells (arrows) with much higher levels of pygo transcripts (H).

Return to article