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

Certain viruses, transposons, and cellular genes have evolved specific sequ ences that induce high levels of specific translational errors. Such "progr ammed misreading" can result in levels of frameshifting or nonsense codon r eadthrough 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 a mong 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 ribosoma l protein mutation and another rRNA mutation) had no effect, Three antisupp ressor rRNA mutations all reduced Ty1 frameshifting; however the antisuppre ssor mutation in the ribosomal protein did not show any effect. Among nonri bosomal mutations, the allosuppressor protein phosphatase mutation enhanced Ty1 frameshifting, whereas the partially inactive prion form of the releas e 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 translat ional machinery. Surprisingly we find that translational suppressors can af fect Ty frameshifting in either direction, whereas antisuppressors have eit her no effect or cause a decrease.