ArticleFolia microbiologica2006
Immunity to killer toxin K1 is connected with the Golgi-to-vacuole protein degradation pathway.
Article in Folia microbiologica, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Extrachromosomally co-encoded toxin-immunity pairs in yeast and their application potential.Applied microbiology and biotechnology · 2026Review
- Expression of the K74 Killer Toxin from Saccharomyces paradoxus Is Modulated by the Toxin-Encoding M74 Double-Stranded RNA 5' Untranslated Terminal Region.Applied and environmental microbiology · 2022Article
- Analysis of Yeast Killer Toxin K1 Precursor Processing via Site-Directed Mutagenesis: Implications for Toxicity and Immunity.mSphere · 2020Article
- Yeast Viral Killer Toxin K1 Induces Specific Host Cell Adaptions via Intrinsic Selection Pressure.Applied and environmental microbiology · 2020Article
- Messenger RNAs of Yeast Virus-Like Elements Contain Non-templated 5' Poly(A) Leaders, and Their Expression Is Independent of eIF4E and Pab1.Frontiers in microbiology · 2019Article
- Article
- Transport according to GARP: receiving retrograde cargo at the trans-Golgi network.Trends in cell biology · 2011Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Killer strains of Saccharomyces cerevisiae producing killer toxin K1 kill sensitive cells but are resistant to their own toxin. It is assumed that in the producer, an effective interaction between the external toxin and its plasma membrane receptor or the final effector is not possible on the grounds of a conformation change of the receptor or its absence in a membrane. Therefore, it is possible that some mutants with defects in intracellular protein transport and degradation can show a suicidal phenotype during K1 toxin production. We have examined these mutants in a collection of S. cerevisiae strains with deletions in various genes transformed by the pYX213+M1 vector carrying cDNA coding for the K1 toxin under the control of the GAL1 promoter. Determination of the quantity of dead cells in colony population showed that (1) the toxin production from the vector did not support full immunity of producing cells, (2) the suicidal phenotype was not connected with a defect in endocytosis or autophagy, (3) deletants in genes VPS1, VPS23, VPS51 and VAC8 required for the protein degradation pathway between the Golgi body and the vacuole exhibited the highest mortality. These results suggest that interacting molecule(s) on the plasma membrane in the producer might be diverted from the secretion pathway to degradation in the vacuole.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.