Decreased peptidyltransferase activity correlates with increased programmed -1 ribosomal frameshifting and viral maintenance defects in the yeast Saccharomyces cerevisiae

Increased efficiencies of programmed -1 ribosomal frameshifting in yeast cells expressing mutant forms of ribosomal protein L3 are unable to maintain the dsRNA "Killer" virus. Here we demonstrate that changes in frameshifting and virus maintenance in these mutants correlates with decreased...

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Bibliographic Details
Published inRNA (Cambridge) Vol. 9; no. 8; pp. 982 - 992
Main Authors Meskauskas, Arturas, Harger, Jason W, Jacobs, Kristi L Muldoon, Dinman, Jonathan D
Format Journal Article
LanguageEnglish
Published United States Copyright 2003 by RNA Society 01.08.2003
Subjects
Alleles
Amino Acid Sequence
Base Sequence
DNA, Fungal
Frameshifting, Ribosomal
Molecular Sequence Data
Peptidyl Transferases - metabolism
Plasmids
RNA, Messenger - genetics
Saccharomyces cerevisiae - enzymology
Saccharomyces cerevisiae - genetics
Saccharomyces cerevisiae - virology
Sequence Homology, Amino Acid
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Summary:Increased efficiencies of programmed -1 ribosomal frameshifting in yeast cells expressing mutant forms of ribosomal protein L3 are unable to maintain the dsRNA "Killer" virus. Here we demonstrate that changes in frameshifting and virus maintenance in these mutants correlates with decreased peptidyltransferase activities. The mutants did not affect Ty1-directed programmed +1 ribosomal frameshifting or nonsense-mediated mRNA decay. Independent experiments demonstrate similar programmed -1 ribosomal frameshifting specific defects in cells lacking ribosomal protein L41, which has previously been shown to result in peptidyltransferase defects in yeast. These findings are consistent with the hypothesis that decreased peptidyltransferase activity should result in longer ribosome pause times after the accommodation step of the elongation cycle, allowing more time for ribosomal slippage at programmed -1 ribosomal frameshift signals.
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Article and publication are at http://www.rnajournal.org/cgi/doi/10.1261/rna.2165803.
Reprint requests to: Jonathan D. Dinman, Department of Cell Biology and Molecular Genetics, Microbiology Building, Room 2135, University of Maryland, College Park, MD 20742, USA; e-mail: dinman@umd.edu; fax: 301-314-9489.
ISSN:1355-8382
1469-9001
DOI:10.1261/rna.2165803