[NSI +] determinant has a pleiotropic phenotypic manifestation that is modulated by SUP35, SUP45, and VTS1 genes

• DOI: 10.1007/s00294-011-0363-1
• Publication Date: 2012-01-03T08:38:59Z
• Authors: Anton A. Nizhnikov; Zalina M. Magomedova; Alexandr A. Rubel; Alexandra M. Kond...; Sergey G. Inge-Ve...; Alexey P. Galkin
• Keywords: 0301 basic medicine; 0303 health sciences; Saccharomyces cerevisiae Proteins; Base Sequence; Prions; Molecular Sequence Data; Gene Dosage; RNA-Binding Proteins; Saccharomyces cerevisiae; 3. Good health; 03 medical and health sciences; Phenotype; Suppression, Genetic; Codon, Nonsense; Gene Expression Regulation, Fungal; Genome, Fungal; Peptide Termination Factors

We recently discovered the novel non-chromosomal determinant in Saccharomyces cerevisiae [NSI(+)] (nonsense suppression inducer), which causes omnipotent nonsense suppression in strains where the Sup35 N-terminal domain is deleted. [NSI(+)] possesses yeast prion features and does not correspond to previously identified yeast prion determinants. Here, we show that [NSI(+)] enhances nonsense codon read-through and inhibits vegetative growth in S. cerevisiae. Using a large-scale overexpression screen to identify genes that impact the phenotypic effects of [NSI(+)], we found that the SUP35 and SUP45 genes encoding the translation termination factors eRF3 and eRF1, respectively, modulate nonsense suppression in [NSI(+)] strains. The VTS1 gene encodes an NQ-enriched RNA-binding protein that enhances nonsense suppression in [NSI(+)] and [nsi(-)] strains. We demonstrate that VTS1 overexpression, like [NSI(+)] induction, causes translational read-through and growth defects in S. cerevisiae.