Targeted mutations cause eclosion defects and shorten life span. (A) A representative image of dsod^G85R/G85R. (B) The wrinkled-wing phenotype of eclosed adult dsod^H71Y/H71Y flies. (C) Homozygous dsod^G51S/G51S, dsod^H71Y/H71Y, dsod^H48R/H48R, and dsod^G85R/G85R flies do not eclose in expected Mendelian ratios. The eclosion rates of heterozygote flies and dsod^G37R/G37R flies are normal. Error bars are SEM. *** P < 0.0001, Fisher’s exact test. Eclosion defects are dosage sensitive for (D) dsod^G85R and (E) dsod^H71Y mutants. Single-copy dsod mutants were analyzed as trans-heterozygotes with dsod^X-16, an allele that deletes the first exon and promoter region. Bars are average eclosion rates from 12 different vials with at least 200 homozygous mutant progeny. Error bars are SEM. *** P < 0.0001, Fisher’s exact test. (F) Life spans were analyzed for dsod mutants and control dsod^{WTloxP/WTLoxP} flies and survivorship was plotted over time. Survival curves represent an average of three life-span trials. *** P < 0.0001, log-rank test. (G) Statistical comparisons of life-span analysis show eclosed dsod^H71Y/H71Y flies have a severely shortened life span, similar to dsod^G51S/G51S. dsod^G85R/G85R flies do not survive to adulthood, thus are excluded from this experiment. All heterozygous mutants we analyzed have a normal life span.