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Encapsidation of yeast killer double-stranded ribonucleic acids: dependence of M on L

K A Bostian, J A Sturgeon, D J Tipper

    Journal of Bacteriology
    |July 1, 1980
    PubMed

    Insights

    Killer toxin production in Saccharomyces cerevisiae is linked to L-dsRNA, which provides essential capsid proteins for M-dsRNA encapsidation. This suggests L-dsRNA plays a crucial role in maintaining the killer phenotype.

    Area of Science:

    • Molecular Biology
    • Yeast Genetics
    • Virology

    Background:

    • Killer toxin production in Saccharomyces cerevisiae is mediated by virus-like particles (VLPs).
    • These VLPs contain double-stranded ribonucleic acid (dsRNA) genomes, specifically L-dsRNA and M-dsRNA.
    • The relationship and functional dependency between these dsRNA elements are not fully understood.

    Purpose of the Study:

    • To investigate the functional relationship between L-dsRNA and M-dsRNA in killer toxin-producing yeast.
    • To determine the role of L-dsRNA in the replication and expression of M-dsRNA and the killer phenotype.
    • To characterize the protein components of the VLPs and their association with dsRNA.

    Main Methods:

    • Isolation of virus-like particles (VLPs) from killer toxin-producing Saccharomyces cerevisiae strains.
    • Quantification and recovery analysis of L-dsRNA and M-dsRNA within VLPs.
    • Identification and characterization of major capsid polypeptides (ScV-P1) in L- and M-dsRNA VLPs.

    Main Results:

    • High recovery rates of both M-dsRNA (95%) and L-dsRNA (87%) were achieved in VLP fractions.
    • The major capsid polypeptide (ScV-P1) was identical in both L- and M-dsRNA VLPs, with 95% found in VLP fractions.
    • L-dsRNA was identified as the gene encoding ScV-P1, essential for M-dsRNA encapsidation.

    Conclusions:

    • L-dsRNA provides the ScV-P1 protein necessary for encapsidating M-dsRNA, establishing a functional link between the two dsRNA genomes.
    • L-dsRNA is directly associated with the killer character and essential for the maintenance or expression of the killer phenotype.
    • The dsRNA genomes and ScV-P1 production appear stringently coupled, suggesting a helper-defective virus-like relationship.

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