Fig. 2.
Loss of dys function decreases the lifespan in flies. (A) Whole fly reverse transcriptase–polymerase chain reaction indicates the abolishment or reduction in dys isoform transcripts. dysExel6184/dyskx43 flies abolish all but Dp117 transcripts, whereas dysExel6184/dys8-2 and dys8-2/dyskx43 mutants have moderately reduced DLPs transcript levels. (B) Adult expression pattern of GMH5-Gal4 driving with GFP expression specifically in the heart (see also Wessells et al., 2004) (bar = 19 μm). (C) Relative expression of dystrophin in cardiac tube of 1-week-old adults presented as ratio of dys to rp49 mRNA. The bar graph shows that the knockdown of all dys isoforms in dysRNAi/24B-Gal4 flies causes a reduction of ∼60%, and ∼40% with the heart-specific dysRNAi/GMH5-Gal4 knockdown. Each value represents the average ± standard error of the mean of four independent experiments. (D) Survival curves of dys mutant females. The knockdown of all dys isoforms in the mesoderm (dysRNAi/24B-Gal4) shows a moderate reduction in longevity similar to the heterozygous deficiencies dysExel6184/+ and dyskx43/+0. In contrast, the heart-specific dys knockdown does not have an effect on lifespan. Dystrophin-like-product-deficient dysExel6184/dyskx43 mutants show dramatically shortened lifespan. It is possible that this transdeficiency deletes additional genes that are contributing to a normal lifespan.