Stansfield, Ian and Eurwilaichitr, Lily and Tuite, Mick F. (1996) Depletion in the levels of the release factor eRF1 causes a reduction in the efficiency of translation termination in yeast. Molecular Microbiology, 20 (6). pp. 1135-1143. ISSN 0950-382X. (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided)
In Saccharomyces cerevisiae, translation termination is mediated by a complex of two proteins, eRF1 and eRF3, encoded by the SUP45 and SUP35 genes, respectively, Mutations in the SUP45 gene were selected which enhanced suppression by the weak ochre (UAA) suppressor tRNA(Ser) SUQ5. In each of four such allosuppressor alleles examined, an in-frame ochre (TAA) mutation was present in the SUP45 coding region; therefore each allele encoded both a truncated eRF1 protein and a full-length eRF1 polypeptide containing a serine missense substitution at the premature UAA codon, The full-length eRF1 generated by UAA readthrough was present at sub-wild-type levels, In an suq5(+) (i.e, non-suppressor) background none of the truncated eRF1 polypeptides were able to support cell viability, with the loss of only 27 amino acids from the C-terminus being lethal, The reduced eRF1 levels in these sup45 mutants did not lead to a proportional reduction in the levels of ribosome-bound eRF3, indicating that eRF3 can bind the ribosome independently of eRF1, A serine codon inserted in place of the premature stop codon at codon 46 in the sup45-22 allele did not generate an allosuppressor phenotype, thereby ruling out this 'missense' mutation as the cause of the allosuppressor phenotype, These data indicate that the cellular levels of eRF1 are important for ensuring efficient translation termination in yeast.
|Subjects:||Q Science > QP Physiology (Living systems) > QP517 Biochemistry|
|Divisions:||Faculties > Science Technology and Medical Studies > School of Biosciences|
|Depositing User:||P. Ogbuji|
|Date Deposited:||06 Mar 1914 15:52|
|Last Modified:||10 Jun 2014 12:52|
|Resource URI:||https://kar.kent.ac.uk/id/eprint/18523 (The current URI for this page, for reference purposes)|