1887

Abstract

Resistance to the low fungal epipolythiodiketopiperazine toxin, gliotoxin, varied threefold between the phytopathogens and Uptake of radiolabelled gliotoxin was rapid and concentration dependent. Uptake by was largely complete within 1 min while the rate of uptake peaked within 10 min for (anastomosis groups 2-2 and 4). Uptake of gliotoxin by was twice that shown by the more resistant A deep rough mutant of , deficient in outer-membrane polysaccharide synthesis, was hypersensitive to gliotoxin, indicating that diffusion barriers play a role in relative sensitivity to gliotoxin. Fungal glutathione levels (reduced and oxidized) did not differ appreciably before or after gliotoxin exposure, indicating that this cytoplasm-based detoxification mechanism was not important in the relative fungal sensitivity to gliotoxin. Binding of the radiolabelled thiol reagents -ethylmaleimide (NEM) and iodoacetic acid to fungal thiol groups was inhibited by gliotoxin. Conversely, the thiol reagents NEM and -chloromercuribenzoic acid inhibited the uptake of radiolabelled gliotoxin. Uptake of radiolabelled amino acids and glucose was reduced by up to 85% by gliotoxin (8 μg ml). It is suggested that the primary mechanism of action of gliotoxin involves selective binding to cytoplasmic membrane thiol groups.

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1988-07-01
2021-05-12
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