Mitochondrial transport and quality control in neurons

We seek to understand the regulatory mechanisms that control the movements of mitochondria in cells. Mitochondria move and undergo fission and fusion in all eukaryotic cells, but the need to supply mitochondria to the far-flung extremities of neurons creates a particular urgency for mitochondrial transport in neurons. Defects in mitochondrial movements can give rise to peripheral neuropathies and degeneration. We and our colleagues have identified a protein complex that includes milton, Miro, and the kinesin-1 heavy chain (KHC) and have shown that this complex is essential for the anterograde ((+)-end directed) transport of mitochondria in neurons. We have determined that multiple mitochondrial inside-out and cytosolic signals converge on Miro to regulate mitochondrial motility. We now propose to further our understanding of the integration of cellular signals that influence mitochondrial motility and quality in neurons. These signaling pathways are crucial to the ability of mitochondria to properly distribute themselves within neuronal compartments and to permit neurons to respond to stresses and changes in activity. Project Number: 1R35GM161519-01 | Fiscal Year: 2026 | NIH Institute/Center: National Institute of General Medical Sciences (NIGMS) | Principal Investigator: XINNAN WANG | Institution: STANFORD UNIVERSITY, STANFORD, CA | Award Amount: $423,500 | Activity Code: R35 | Study Section: Special Emphasis Panel[ZRG1 CDB-N (55)] View on NIH RePORTER: https://reporter.nih.gov/project-details/11260559