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Yeast dsRNA viruses: replication and killer phenotypes
Author(s) -
Tipper D. J.,
Schmitt M. J.
Publication year - 1991
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.1991.tb02078.x
Subject(s) - biology , replication (statistics) , phenotype , rna silencing , virology , yeast , genetics , rna , gene , rna interference
Summary The cytoplasmic L‐A dsRNA virus of Saccharomyces cerevisiae consists of a 4.5kb dsRNA and the two gene products it encodes: the capsid (cap) and at least one copy of the capsid–polymerase (cap–pol) fusion protein. Virion cap–pol catalyses transcription of the plus (sense)‐strand; this is extruded from the virus and serves as messenger for synthesis of cap and cap–pol. Nascent cap–pol binds to a specific domain in the plus strand to initiate encapsidation and then catalyses minus‐strand synthesis to complete the replication cycle. Products of at least three host genes are required for replication, and virus copy number is kept at tolerable levels by the SKI antivirus system. S. cerevisiae killer viruses are satellite dsRNAs that use a similar encapsidation domain to parasitize the L‐A replication machinery. They encode precursors of secreted polypeptide toxins and immunity (specific resistance) determinants and are self‐selecting. Three unique killer types, K 1 , K 2 and K 28 , are currently recognized. They are distinguished by an absence of cross‐immunity and by toxin properties and lethal mechanisms; while K 1 and K 2 toxins bind to cell‐wall glucan and disrupt membrane functions, K 28 toxin binds to mannoprotein and causes inhibition of DNA synthesis.