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Mcm1 is an essential Q/N-rich transcription factor. Q/N-rich proteins interact with each other, and many affect the [<i>PSI</i>⁺] prion formed by the translation termination factor Sup35 (eRF3). We found that transient <i>MCM1</i> overexpression increased nonsense suppression in [<i>PSI</i>⁺] strains and <i>SUP35</i> transcription. As we had discovered similar effects of another Q/N-rich transcription factor, Sfp1, here we focus on the roles of Mcm1 and Sfp1 in <i>SUP35</i> expression, as well as on the effects of Sfp1 on the expression of the gene encoding another release factor, Sup45 (eRF1). Mutations in the <i>SUP35</i> promoter showed that none of the potential Mcm1 binding sites affected the Sup35 protein level or nonsense suppression, even during <i>MCM1</i> overexpression. Mcm1 itself neither formed aggregates in vivo nor affected Sup35 aggregation. In contrast, a mutation in the Sfp1-binding site decreased Sup35 production and [<i>PSI</i>⁺] toxicity of excess Sfp1. Mutation of the Sfp1 binding site in the <i>SUP45</i> promoter lowered <i>SUP45</i> expression and increased nonsense suppression even more drastically. Our data indicate that the mechanisms of Mcm1 and Sfp1 action differ. While Mcm1 seems unlikely to directly regulate <i>SUP35</i> expression, Sfp1 appears to act through its binding sites and to directly activate <i>SUP35</i> expression, which in turn may influence the [<i>PSI</i>⁺] prion phenotype and toxicity.