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Genetics, Vol 141, 481-489, Copyright © 1995
INVESTIGATIONS |
Increased Expression of Saccharomyces cerevisiae Translation Elongation Factor 1{alpha} Bypasses the Lethality of a TEF5 Null Allele Encoding Elongation Factor 1{beta}
T. G. Kinzy and J. L. Woolford-Jr.
Present address: Department of Molecular Genetics and Microbiology, UMDNJ Robert Wood Johnson Medical School, 675 Hoes Lane, Piscataway, NJ 08854-5635.
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.
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