Disease relevance of gas-1

• The hypersensitivity of animals with a mutation in the gas-1 gene may be caused by a direct anesthetic effect on a mitochondrial protein or secondary effects at other sites caused by mitochondrial dysfunction [1].
• Mutations in the mev-1 and gas-1 genes of the nematode Caenorhabditis elegans render animals hypersensitive to oxygen and paraquat, and lead to premature aging [2].

High impact information on gas-1

• An increase in Complex II-dependent metabolism also is seen in mitochondria from gas-1 animals [3].
• 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 [3].
• The halothane concentrations needed to immobilize 50% of N2 or gas-1 animals, respectively, did not reduce oxidative phosphorylation to identical rates in the two strains [4].
• At equal halothane concentrations, complex I activity but not complex II activity was lower in mitochondria from mutant (gas-1) animals than from wild-type (N2) animals [4].
• In air, adenosine triphosphate concentrations were similar for N2 and gas-1 but were decreased in the presence of halothane only in gas-1 animals [4].

Biological context of gas-1

• A mutation in a subunit of complex I of the mitochondrial electron transport chain (gas-1) causes Caenorhabditis elegans to be hypersensitive to volatile anesthetics and oxygen as well as shortening lifespan [5].
• Suppressors of gas-1 increased rates of oxidative phosphorylation, decreased oxidative damage to mitochondrial proteins and increased lifespan [5].
• Since both gas-1 and mev-1 encode subunits of electron transport chain complexes, these data illustrate how mitochondrial perturbations can impact signal transduction pathways [2].
• Effect of oxidative stress on translocation of DAF-16 in oxygen-sensitive mutants, mev-1 and gas-1 of Caenorhabditis elegans [2].

Associations of gas-1 with chemical compounds

• CONCLUSIONS: The difference in ethanol sensitivities between gas-1 and wild-type nematodes results solely from altered complex I function [6].

Physical interactions of gas-1

• In the nematode Caenorhabditis elegans, mutations have been previously isolated that affect the activities of Complex I (gas-1) and Complex II (mev-1), two of the five membrane-bound complexes that control electron flow in mitochondrial respiration [7].

Other interactions of gas-1

• Lifespans of gas-1 and mev-1 were decreased compared with N2, while that of clk-1 was increased [5].

Analytical, diagnostic and therapeutic context of gas-1

• The feeding method was employed to deliver dsRNA from the fourth subunit (ceSDHA) to wild-type, mev-1 (mutated in ceSDHC of complex II), and gas-1 animals (mutated in a complex I gene) [8].

References