PREY

SUP35

GST1, PNM2, SAL3, SUF12, SUP2, SUP36, translation termination factor GTPase eRF3, eRF3, [PSI(+)], [PSI], L000002200, YDR172W
Translation termination factor eRF3; has a role in mRNA deadenylation and decay; altered protein conformation creates the [PSI(+)] prion that modifies cellular fitness, alters translational fidelity by affecting reading frame selection, and results in a nonsense suppressor phenotype; many stress-response genes are repressed in the presence of [PSI(+)]
GO Process (2)
GO Function (2)
GO Component (2)
Saccharomyces cerevisiae (S288c)

Dosage Lethality

A genetic interaction is inferred when over expression or increased dosage of one gene causes lethality in a strain that is mutated or deleted for another gene.

Publication

Polyglutamine toxicity is controlled by prion composition and gene dosage in yeast.

Gong H, Romanova NV, Allen KD, Chandramowlishwaran P, Gokhale K, Newnam GP, Mieczkowski P, Sherman MY, Chernoff YO

Polyglutamine expansion causes diseases in humans and other mammals. One example is Huntington's disease. Fragments of human huntingtin protein having an expanded polyglutamine stretch form aggregates and cause cytotoxicity in yeast cells bearing endogenous QN-rich proteins in the aggregated (prion) form. Attachment of the proline(P)-rich region targets polyglutamines to the large perinuclear deposit (aggresome). Aggresome formation ameliorates polyglutamine cytotoxicity in ... [more]

PLoS Genet. Apr. 01, 2012; 8(4);e1002634 [Pubmed: 22536159]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: dosage lethality (APO:0000172) [dosage lethality (APO:0000172)]

Additional Notes

  • figure 1. Overexpression of Htt-103Q construct is synthetic lethal with either the prion form of Sup35 protein ([PSI+]) or form of Rnq1 protein ([PIN+]); while Overexpression of Htt-103Q construct is synthetic lethal with only the prion form of Sup35 protein ([PSI+]).

Curated By

  • BioGRID