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A mutation in mitochondrial complex I increases ethanol sensitivity in Caenorhabditis elegans.
Ernst-Bernhard Kayser1, Charles L Hoppel, Phil G Morgan
1Department of Anesthesiology, University Hospitals, Cleveland, Ohio 44106, USA.
Alcoholism, Clinical and Experimental Research
|April 25, 2003
Summary
A mutation in the gas-1 gene increases ethanol sensitivity in C. elegans by altering complex I function. This change in complex I activity controls the nematode's transition from mobility to immobility when exposed to ethanol.
Area of Science:
- Mitochondrial biology
- Genetics
- Neuroscience
Background:
- The gas-1 gene in C. elegans encodes a subunit of mitochondrial complex I.
- gas-1 mutations increase ethanol sensitivity and decrease complex I metabolism.
Purpose of the Study:
- To investigate the effects of ethanol on mitochondrial oxidative phosphorylation in wild-type and gas-1 mutant C. elegans.
- To determine the role of complex I in ethanol-induced immobility.
Main Methods:
- Isolated mitochondria from wild-type and gas-1 C. elegans strains.
- Measured complex I, II, and III-dependent oxidative phosphorylation in the presence of ethanol.
- Assessed reversibility of ethanol's effects and visualized mitochondrial structure via electron microscopy.
Main Results:
- Ethanol inhibited all three complexes in wild-type mitochondria at immobilizing concentrations.
- gas-1 mitochondria showed lower complex I and higher complex II activity than wild-type.
- Ethanol's inhibitory effects on mitochondria were reversible.
Conclusions:
- Altered complex I function in gas-1 mutants is solely responsible for increased ethanol sensitivity.
- A threshold of complex I activity dictates C. elegans immobility in response to ethanol.