UCP2 Regulates Embryonic Neurogenesis via ROS-Mediated Yap Alternation in the Developing Neocortex

• DOI: 10.1002/stem.2605
• Publication Date: 2017-03-09T10:38:27Z
• Authors: Fen Ji; Tianjin Shen; Wenzheng Zou; Jianwei Jiao
• Keywords: Neocortex

Abstract Mitochondrial metabolism is a fundamental process in tissue development. How this play functions embryonic neurogenesis remains largely unknown. Here, we show that mitochondrial uncoupling protein 2 (UCP2) regulates the by inhibiting production of reactive oxygen species (ROS), which affect proliferation progenitors. In brains UCP2 knockdown or condition knockout mice, progenitors significantly increased, while differentiation reduced. Furthermore, identify Yap response UCP2-mediated ROS production. When inactive, increased. The amount increased as degradation through ubiquitin–proteasome proteolytic pathway decreased. defect caused depression can be rescued downregulation. Collectively, our results demonstrate ROS-mediated alternation, thus shedding new sight on involved neurogenesis.