Mitochondria, the power plants of the cell, come equipped with their own small genome. It is a remnant, left over from the ancient symbiotic bacteria that later became mitochondria, containing the few genes that failed to migrate to the cell nucleus over evolutionary time. Every species exhibits numerous different mitochondrial haplogroups, and given that these lead to variance in the performance and activities of mitochondria, one might be tempted to think that some haplogroups are objectively better than others. This study suggests that advantages and disadvantages vary by environment and diet, however, which might explain why evolution has selected for multiple haplogroups rather than one dominant haplogroup.
This is all interesting, but none of it stops the research community from engineering a globally better-than-natural human mitochondrial genome, and then copying it into the cell nucleus as a backup to prevent the well-known contribution of mitochondrial DNA damage to aging. Further, nothing stops us from keeping the haplogroups we have and rendering the effects of variants small and irrelevant through the development of other forms of enhancement biotechnology. The natural world handed over to us after billions of years of evolution is a starting point, not the bounds of the possible.
Mitochondrial DNA (mtDNA) and the dietary macronutrient ratio are known to influence a wide range of phenotypic traits including longevity, fitness and energy production. Commonly mtDNA mutations are posited to be selectively neutral or reduce fitness and, to date, no selectively advantageous mtDNA mutations have been experimentally demonstrated in adult female Drosophila. Here we propose that a ND V161L mutation interacted with diets differing in their macronutrient ratios to influence organismal physiology and mitochondrial traits, but further studies are required to definitively show no linked mtDNA mutations are functionally significant.
We utilized two mtDNA types (mitotypes) fed either a 1:2 Protein: Carbohydrate (P:C) or 1:16 P:C diet. When fed the former diet, Dahomey females harboring the V161L mitotype lived longer than those with the Alstonville mitotype and had higher climbing, basal reactive oxygen species (ROS) and elevated glutathione S-transferase E1 expression. The short lived Alstonville females ate more, had higher walking speed and elevated mitochondrial functions as suggested by respiratory control ratio (RCR), mtDNA copy number and expression of mitochondrial transcription termination factor 3. In contrast, Dahomey females fed 1:16 P:C were shorter lived, had higher fecundity, walking speed, and mitochondrial functions. They had reduced climbing.
This result suggests that mtDNA cannot be assumed to be a strictly neutral evolutionary marker when the dietary macronutrient ratio of a species varies over time and space and supports the hypothesis that mtDNA diversity may reflect the amount of time since the last selective sweep rather than strictly demographic processes.