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Tae Hoon Lee^1,, Ji Young Mun^2,, Sung Min Han¹, Gyesoon Yoon³, Sung Sik Han^2,* and Hyeon-Sook Koo^1,*

¹ Department of Biochemistry, College of Science, Yonsei University, Seoul 120-749, Republic of Korea
² School of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Republic of Korea
³ Department of Biochemistry, School of Medicine and Department of Molecular Science and Technology, The Graduate School, Ajou University, Suwon 443-721, Republic of Korea

Deficiency of the Caenorhabditis elegans protein, DIC-1, located in the inner membrane of mitochondria produces an abnormal mitochondrial morphology. The mechanism by which DIC-1 controls the topology of the inner membrane was investigated by transiently over-expressing DIC-1 in C. elegans. Cryo-electron microscopy showed that DIC-1 over-expression greatly increased the number and fractional area of mitochondrial cristae, suggesting that DIC-1 actively participates in cristae formation. These morphological changes were accompanied by increases in the oxygen consumption rate and ATP content of C. elegans worms, and decreases in reactive oxygen species (ROS) and sensitivity to paraquat. DIC-1 knockdown induced the opposite changes in ATP, ROS and paraquat-sensitivity. The ability of DIC-1 to increase cristae formation and secondarily, oxidative phosphorylation, suggests a potential use of this factor to control mitochondrial activity.

The authors made equal contributions to the work.

^* Correspondence: kooh{at}yonsei.ac.kr or sshan{at}korea.ac.kr