Fig. 1. ey alleles isolated as dominant Enhancers of eye loss induced by ectopic expression from the HSPB^sy transgene. Dose-sensitive eye loss induced by HSPB^sy. (A-C) Heads of flies carrying one, two or four HSPB^sy copies, respectively. (B) Two copies; slightly reduced eye (arrowhead). (C) Four copies; complete eye deletion (arrowhead). The genetic screen selected for female progeny carrying two HSPB^sy copies (B) or an interacting Enhancer locus, which yields an eye loss resembling four copies (C). (D) Strength and specificity of the pb-ey genetic interaction. Four new alleles (ey^JD, ey^D1Da, ey¹¹, ey^EH), two previously isolated ey loss-of-function alleles [ey² and Df(4)BA], and several alleles of other genes implicated in eye differentiation, were tested for dose-sensitive interactions with HSPB^sy. Males harboring one HSPB^sy copy and heterozygous for mutant alleles of the eye development genes sine oculis (so), eyes absent (eya), eye gone (eyg) or ey were crossed with homozygous HSPB^sy females. Maximal eye loss expected is 50% in the resulting female progeny (harboring two copies of HSPB^sy) because half should carry the eye gene mutation. Several allele names are shortened: eya^c1 is eya^clift1 (from L. Zipursky), eyg^M is eyg^M3-12 (from H. Sun) and ey^D1 is ey^D1Da (this paper). (E,F). All four newly isolated ey alleles should yield truncated forms of the EY protein. (E) Representations of wild-type EY protein and of the proteins encoded by ey^JD, ey^D1Da (Callaerts et al., 2001), or predicted based on the sequences of ey¹¹ and ey^EH (this paper). HD, homeodomain; PD, paired domain. (F) Sequences of wild-type ey and of the mutant lesions in ey¹¹ and ey^EH. Modifications in the mutant sequences are underlined, exon or intron boundaries are indicated by arrows, and a new stop codon by `-'.