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DIC‐1 over‐expression enhances respiratory activity in Caenorhabditis elegans by promoting mitochondrial cristae formation
Author(s) -
Lee Tae Hoon,
Mun Ji Young,
Han Sung Min,
Yoon Gyesoon,
Han Sung Sik,
Koo HyeonSook
Publication year - 2009
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2008.01276.x
Subject(s) - caenorhabditis elegans , biology , microbiology and biotechnology , mitochondrion , paraquat , oxidative phosphorylation , reactive oxygen species , gene knockdown , inner mitochondrial membrane , inner membrane , biochemistry , apoptosis , gene
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.