Rubicon regulates mitochondria metabolism through p22phox

Abstract

The run / cysteine-rich-domain-containing Beclin1-interacting autophagy protein (Rubicon) is a key player in the immune response and autoimmunity. Rubicon has canonical and non-canonical autophagy functions, for that reason, it is a candidate for therapeutic potent. According to recent studies, Rubicon interacts with p22phox to cause reactive oxygen species (ROS) in a dose-dependent manner. However, knowledge about the correlation between Rubicon and mitochondrial ROS (mtROS) is lacking. In this study, we confirmed that Rubicon interacts with p22phox in murine macrophages and their complex induces to not only cytosolic ROS but also mtROS. Furthermore, we showed translocation of the complex and finally Rubicon had negative effects on mitochondrial activity and biogenesis through impairment of mitochondrial complex Ⅲ. Taken together, our results suggest that regulation of Rubicon expression is important strategy of mitochondrial metabolism.