Partial Inactivation of Translation Termination Factors Causes Suppression of Frameshift Mutations in the Yeast Saccharomyces cerevisiae

Partial Inactivation of Translation Termination Factors Causes Suppression of Frameshift... Special search for frameshift mutations, which are suppressed by the cytoplasmic [PSI] factor and by omnipotent nonsense suppressors (recessive mutations in theSUP35and SUP45genes), partially inactivating a translation termination complex, was initiated in theLYS2gene in the yeast Saccharomyces cerevisiae.Mutations were obtained after exposure to UV light and treatment with a mixture of 1,6- and 1,8-dinitropyrene (DNP). This mixture was shown to induce mutations of the frameshift type with a high frequency. The majority of these mutations were insertions of one A or T, which is in good agreement with the data obtained in studies of DNP-induced mutagenesis in other eukaryotes. Frameshift suppression was shown on the example of the mutation obtained in this work (lys2-90), which carried the insertion of an extra T in the sequence of five T. This frameshift suppression was first shown to occur in the presence of the [PSI] factor (i.e., due to the prionization of the translation release factor eRF3) and as a result of mutations in genes SUP35orSUP45, which partially inactivate translation termination factors eRF3 and eRF1, respectively. Alternative mechanisms of programmed translational frameshifting in the course of translation and the possibility of enhancing the effectiveness of such frameshifting in the presence of the [PSI] factor are considered. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Russian Journal of Genetics Springer Journals

Partial Inactivation of Translation Termination Factors Causes Suppression of Frameshift Mutations in the Yeast Saccharomyces cerevisiae

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Publisher
Kluwer Academic Publishers-Plenum Publishers
Copyright
Copyright © 2001 by MAIK “Nauka/Interperiodica”
Subject
Biomedicine; Human Genetics
ISSN
1022-7954
eISSN
1608-3369
D.O.I.
10.1023/A:1016606412918
Publisher site
See Article on Publisher Site

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