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Translational suppressors and antisuppressors alter the efficiency of the Ty1 programmed translational frameshift

Published online by Cambridge University Press:  01 November 1999

C.L. BURCK
Affiliation:
Laboratory for Molecular Biology, Department of Biological Sciences, University of Illinois at Chicago, Chicago, Illinois 60607, USA Present address: Department of Cancer Cell Biology, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
Y.O. CHERNOFF
Affiliation:
Laboratory for Molecular Biology, Department of Biological Sciences, University of Illinois at Chicago, Chicago, Illinois 60607, USA Present address: School of Biology, Georgia Institute of Technology, Atlanta, Georgia 30332, USA.
R. LIU
Affiliation:
Laboratory for Molecular Biology, Department of Biological Sciences, University of Illinois at Chicago, Chicago, Illinois 60607, USA Present address: Aaron Diamond AIDS Research Center, New York, New York 10016, USA.
P.J. FARABAUGH
Affiliation:
Department of Biological Sciences, University of Maryland–Baltimore County, Baltimore, Maryland 21250, USA
S.W. LIEBMAN
Affiliation:
Laboratory for Molecular Biology, Department of Biological Sciences, University of Illinois at Chicago, Chicago, Illinois 60607, USA
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Abstract

Certain viruses, transposons, and cellular genes have evolved specific sequences that induce high levels of specific translational errors. Such “programmed misreading” can result in levels of frameshifting or nonsense codon readthrough that are up to 1,000-fold higher than normal. Here we determine how a number of mutations in yeast affect the programmed misreading used by the yeast Ty retrotransposons. These mutations have previously been shown to affect the general accuracy of translational termination. We find that among four nonsense suppressor ribosomal mutations tested, one (a ribosomal protein mutation) enhanced the efficiency of the Ty1 frameshifting, another (an rRNA mutation) reduced frameshifting, and two others (another ribosomal protein mutation and another rRNA mutation) had no effect. Three antisuppressor rRNA mutations all reduced Ty1 frameshifting; however the antisuppressor mutation in the ribosomal protein did not show any effect. Among nonribosomal mutations, the allosuppressor protein phosphatase mutation enhanced Ty1 frameshifting, whereas the partially inactive prion form of the release factor eRF3 caused a slight decrease, if any effect. A mutant form of the other release factor, eRF1, also had no effect on frameshifting. Our data suggest that Ty frameshifting is under the control of the cellular translational machinery. Surprisingly we find that translational suppressors can affect Ty frameshifting in either direction, whereas antisuppressors have either no effect or cause a decrease.

Type
Research Article
Copyright
1999 RNA Society

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