Abstract

Due to the maternal inheritance of mitochondria, many of the mitochondrial genes and targeted proteins are optimized in a sex‐dependent manner, favoring females. In turn, this generates a biological power‐play between the sexes. One example is the mitochondrial stress response protein, the Lon protease. Our work in the model organism Drosophila melanogaster, has uncovered a sexual difference in Lon expression. A major hallmark of this sexual dimorphism is the ability of females, pre‐treated with hydrogen peroxide to adapt (measured by increased survival time) compared to non‐pretreated females, when subsequently exposed to a lethal dose of hydrogen peroxide. In contrast males, regardless if they are pre‐treated or only challenged, show no adaptation. As well, the removal of Lon from females prevents adaptation, with no impact upon males. In addition, Lon protein expression and activity is only inducible in a sex‐dependent manner. Based on our findings, we attribute these differences to the unique Lon protein banding variation that we have identified in males and females.Support or Funding InformationNational Science Foundation Graduate Research Fellowship; NIH/NIEHS RO1ES003598 (PI Davies, K.J.A.)

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