METABOLISM AND BIOENERGETICS
Mitochondrial Expression and Function of GAS-1 in Caenorhabditis elegans

https://doi.org/10.1074/jbc.M011066200Get rights and content
Under a Creative Commons license
open access

A mutation in the gene gas-1 alters sensitivity to volatile anesthetics, fecundity, and life span in the nematode Caenorhabditis elegans. gas-1 encodes a close homologue of the 49-kDa iron protein subunit of Complex I of the mitochondrial electron transport chain from bovine heart.gas-1 is widely expressed in the nematode neuromuscular system and in a subcellular pattern consistent with that of a mitochondrial protein. Pharmacological studies indicate thatgas-1 functions partially via presynaptic effects. In addition, a mutation in the gas-1 gene profoundly decreases Complex I-dependent metabolism in mitochondria as measured by rates of both oxidative phosphorylation and electron transport. An increase in Complex II-dependent metabolism also is seen in mitochondria from gas-1 animals. There is no apparent alteration in physical structure in mitochondria from gas-1nematodes compared with those from wild type. These data indicate thatgas-1 is the major 49-kDa protein of complex I and that the GAS-1 protein is critical to mitochondrial function in C. elegans. They also reveal the importance of mitochondrial function in determining not only aging and life span, but also anesthetic sensitivity, in this model organism.

Cited by (0)

Published, JBC Papers in Press, February 20, 2001, DOI 10.1074/jbc.M011066200

*

This work was supported in part by National Institutes of Health Grants GM58881 and GM45402 (to M.M.S. and P.G.M.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Supported by the Veterans Administration Hospital Medical Services and by National Institutes of Health Grant PO1 AG15885.