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Fig. 1. Uba1 mutants are autonomous suppressors of GMR-hid-induced apoptosis. (A) The unmodified small eye phenotype caused by GMR-hid ey-FLP (GheF). (B,C) The GheF phenotype is moderately strongly suppressed by Uba1 alleles at 25°C. Genotype: GheF; FRT42D Uba1^H33 and Uba1^H42/FRT42 P[w⁺], respectively. (D) The unmodified small eye phenotype caused by a GMR-hid transgene that lacks the white⁺ marker gene (GMR-hid[w^-]). Note, the GMR-hid transgene in (A) carries the white⁺ minigene. Genotype: ey-FLP; GMR-hid[w^-]. (E,F) The suppression of GMR-hid[w^-] is mediated by Uba1 mutant tissue which is phenotypically white^-. Flies were incubated at 25°C. Genotype: ey-FLP; FRT42D Uba1^H33and Uba1^H42/FRT42D P[w⁺]; GMR-hid[w^-], respectively. (G) Outline of the Uba1 protein and locations of the mutations of the Uba1 alleles isolated in this study. The red box indicates the internal deletion of Uba1^H42. The yellow boxes mark the Thif domains, and the blue boxes highlight the location of the catalytic Ube domains. (H) A highly conserved stretch of residues, incorporating Pro884 is present in a range of species from yeast to humans. Dm, Drosophila melanogaster; Sc, Saccharomyces cerevisiae; Mm, Mus musculus; Xl, Xenopus laevis; Hs, Homo sapiens. (I) RT-PCR of mRNA isolated from wild-type and Uba1^H42 mutant larvae revealing an aberrantly spliced product. This results in an in frame deletion from amino acid residue 162 to 255 of Uba1^H42 (see G). Primers were directed against the N-terminal third of Uba1.

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