Mitochondrial Reactive Oxygen Species Modulate Mosquito Susceptibility to <em>Plasmodium</em> Infection

<div><h3>Background</h3><p>Mitochondria perform multiple roles in cell biology, acting as the site of aerobic energy-transducing pathways and as an important source of reactive oxygen species (ROS) that modulate redox metabolism.</p> <h3>Methodology/Principal Findings</h3><p>We demonstrate that a novel member of the mitochondrial transporter protein family, <em>Anopheles gambiae</em> mitochondrial carrier 1 (AgMC1), is required to maintain mitochondrial membrane potential in mosquito midgut cells and modulates epithelial responses to <em>Plasmodium</em> infection. AgMC1 silencing reduces mitochondrial membrane potential, resulting in increased proton-leak and uncoupling of oxidative phosphorylation. These metabolic changes reduce midgut ROS generation and increase <em>A. gambiae</em> susceptibility to <em>Plasmodium</em> infection.</p> <h3>Conclusion</h3><p>We provide direct experimental evidence indicating that ROS derived from mitochondria can modulate mosquito epithelial responses to <em>Plasmodium</em> infection.</p> </div>