Mitochondria and copper homeostasis in plants

• Copper is essential for plant cells but also toxic when present in excess.
• Copper is required in mitochondria for the assembly of cytochrome c oxidase (COX).
• Several mitochondrial proteins participate in copper insertion into COX.
• Some of these proteins also participate in the modulation of copper homeostasis.
• They may act as signaling molecules linking mitochondria to the rest of the cell.

Copper (Cu) and other transition metals are essential for living organisms but also toxic when present in excess. To cope with this apparent paradox, organisms have developed sophisticated mechanisms to acquire, transport and store these metals. Particularly, plant mitochondria require Cu for the assembly and function of cytochrome c oxidase (COX), the terminal enzyme of the respiratory chain. COX assembly is a complex process that requires the action of multiple factors, many of them involved in the delivery and insertion of Cu into the enzyme. In this review, we summarize what is known about the processes involved in Cu delivery to mitochondria and how these processes impact in Cu homeostasis at the cellular level. We also discuss evidence indicating that metallochaperones involved in COX assembly play additional roles in signaling pathways related to changes in Cu and redox homeostasis and the response of plants to stress. We propose that cysteine-rich proteins present in the mitochondrial intermembrane space are excellent candidates as sensors of these changes and transducers of signals originated in the organelle to the rest of the cell.