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Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance
Published on: January 3, 2012
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Immunity to K1 killer toxin: internal TOK1 blockade
F Sesti1, T M Shih, N Nikolaeva
1Departments of Pediatrics and Cellular and Molecular Physiology, Boyer Center for Molecular Medicine, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06536, USA.
Cell
|June 8, 2001
Summary
Killer yeast cells resist their own toxin by using internal K1 toxin to block TOK1 channels. This prevents external toxin from activating the channels, thus protecting the cells from potassium leakage and death.
Area of Science:
- Microbiology
- Molecular Biology
- Yeast Genetics
Background:
- Saccharomyces cerevisiae killer strains produce K1 toxin, mediated by RNA viruses, to eliminate sensitive yeast.
- External K1 toxin activates TOK1 potassium channels in sensitive yeast, causing potassium efflux and cell death.
Purpose of the Study:
- To elucidate the mechanism by which K1 killer yeast cells achieve self-resistance to their own toxin.
- To investigate the role of internal K1 toxin in modulating TOK1 channel activity.
Main Methods:
- Electrophysiological analysis of TOK1 channel activity in yeast plasma membranes.
- Biochemical assays to assess K1 toxin interaction with TOK1 channels.
- Genetic manipulation of K1 toxin and TOK1 channel expression in Saccharomyces cerevisiae.
Main Results:
- Internal K1 toxin directly inhibits TOK1 channel function.
- Internal K1 toxin prevents the activation of TOK1 channels by external K1 toxin.
- This inhibition mechanism confers resistance to K1 toxin in killer yeast cells.
Conclusions:
- Yeast killer cells possess an intrinsic self-resistance mechanism involving internal K1 toxin.
- Internal K1 toxin acts as a negative regulator of TOK1 channels, preventing autotoxicity.
- The findings reveal a novel molecular strategy for toxin self-tolerance in microbial systems.
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