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Genotype to phenotype: Diet-by-mitochondrial DNA haplotype interactions drive metabolic flexibility and organismal fitness

Fig 5

Corroboration that the complex I mutation in Dahomey drives the population cage results.

(A) Adding rotenone to the Alstonville diet created a Dahomey phenocopy. This phenocopy developed more quickly than controls when fed the 1:16 P:C food showing that partial inhibition of complex I was beneficial. Adding rotenone to the Dahomey fly food created a disease model and these larvae developed more slowly on both diets (n = 5 biological rep/mitotype/diet with and without rotenone treatment). (B) Complex I activity was decreased in the phenocopy, mimicking the Dahomey mitotype (n = 7 biological rep/mitotype/diet without rotenone treatment and 6 biological rep/mitotype/diet with rotenone treatment). (C) SOD activity increased in rotenone-treated larvae. On both foods, SOD activity in the phenocopy was not different from the Dahomey mitotype (n = 5 biological rep/mitotype/diet with and without rotenone treatment). (D) Larval development times of D. melanogaster harbouring the Madang (with the V161L ND4 mutation) and the Victoria Falls (without the ND4 mutation) mitotypes shows the same flip in development times as Dahomey and Alstonville (n = 6 bottles/mitotype/diet). Plotted data were meanĀ± s.e.m. * p< 0.05 and ** p< 0.001, as calculated by t-tests (see text). Note: complete post-hoc analyses including all treatments for panels A-C are presented in S5 Fig.

Fig 5