Increased expression of Saccharomyces cerevisiae translation elongation factor 1α bypasses the lethality of a TEF5 null allele encoding elongation factor 1β

Abstract

Translation elongation factor 1β (EF-1β) catalyzes the exchange of bound GDP for GTP on EF-1α. The lethality of a null allele of the TEF5 gene encoding EF-1β in Saccharomyces cerevisiae was suppressed by extra copies of the TEF2 gene encoding EF-1α. The strains with tef5::TRP1 suppressed by extra copies of TEF2 were slow growing, cold sensitive, hypersensitive to inhibitors of translation elongation and showed increased phenotype suppression of +1 frameshift and UAG nonsense mutations. Nine dominant mutant alleles of TEF2 that cause increased suppression of frameshift mutations also suppressed the lethality of tef5::TRP1. Most of the strains in which tef5::TRP1 is suppressed by dominant mutant alleles of TEF2 grew more slowly and were antibiotic sensitive than strains with tef5::TRP1 suppressed by wild-type TEF2. Two alleles, TEF2-4 and TEF2-10, interact with tef5::TRP1 to produce strains that showed doubling times similar to tef5::TRP1 strains containing extra copies of wild-type TEF2. These strains were less cold sensitive drug sensitive and corresponding less efficient suppressors of +1 frameshift mutations. These phenotypes indicate that translation and cell growth are highly sensitive to changes in EF-1α and EF-1β activity.