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

Fig 10

Tests of hypotheses using other sugars and inhibitors.

Dietary modification of the 1:16 P:C diet with replacement of sugars (sucrose was the dietary sugar for the Control) and inhibitors. Replacement sugars were sorbitol, fructose, mannose, fucose, xylose, and gluconate (n = 4 rep/mitotype).The inhibitors were Epalrestat (Polyol pathway) (n = 5 rep/mitotype), and Etomoxir (β -oxidation) (n = 5 rep/mitotype). More Dahomey than Alstonville flies eclosed in a 3 d window when fed the control diet, as well as diets containing sorbitol, fructose, mannose, and fucose. Fewer Dahomey flies eclosed in a 3 d window when fed gluconate. There was no difference in the number of flies eclosing in 3 days between mitotypes when xylose was the dietary sugar or when Epalrestat or Etomoxir was added to the diet. * p< 0.05; ** p< 0.01, *** p<0.001 as determined by t-tests (see text). Dunnett’s tests compared Dahomey females fed the control diet to diets supplemented with inhibitors or the control diet compared with other sugars • p< 0.05 (see text).

Fig 10

doi: https://doi.org/10.1371/journal.pgen.1007735.g010