Mitochondrial Dysfunction and Innate Immunity in Drosophila melanogaster

Age has long been linked to mitochondrial function. As we age, mitochondrial integrity declines, resulting in inefficient respiration, decreased membrane potential and “leakage” of mitochondrial components into the cytoplasm. Aging has also been linked to dysregulation of innate immune signaling, leading to inflammation and a reduction in response to acute infection. More recently, research has implicated mtDNA as a potential upstream signal for innate immune responses, suggesting a link between these two processes thought to drive aging. Preliminary data from the Wang lab has shown that in Drosophila, mtDNA depletion leads to upregulation of the innate immune response. Here, we are validating those findings in a fly that induces mtDNA depletion in a heat-controlled manner, using RT-qPCR to measure expression of Diptericin—an antimicrobial peptide whose expression increases during the fruit fly innate immune response.