INCREASED EXPRESSION OF SACCHAROMYCES-CEREVISIAE TRANSLATION ELONGATION-FACTOR 1-ALPHA BYPASSES THE LETHALITY OF A TEF5 NULL ALLELE ENCODING ELONGATION-FACTOR 1-BETA

Translation elongation factor 1 beta (EF-1 beta) catalyzes the exchange of bound GDP for GTP on EF-1 alpha. The lethality of a null allele of the TEF5 gene encoding EF-1 beta in Saccharomyces cerevisiae was suppressed by extra copies of the TEF2 gene encoding EF-1 alpha. 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 phenotypic 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 more 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 correspondingly less efficient suppressors of +1 frameshift mutations. These phenotypes indicate that translation and cell growth are highly sensitive to changes in EF-1 alpha and EF-1 beta activity.