The SAL4 gene of the yeast Saccharomyces cerevisiae encodes a novel translation factor (Sal4p) involved in maintaining translational fidelity. Using a polyclonal antibody raised against a Sal4p-beta-galactosidase fusion protein, Sal4p was shown to be almost exclusively associated with the ribosomal fraction. Even when the ribosomes were treated with 0.8 M KCl, only low levels of Sal4p were detected in the post-ribosomal supernatant, suggesting a very strong affinity between Sal4p and the ribosome. Analysis of the distribution of Sal4p in the ribosomal population revealed that it was principally associated with 40S subunits, monosomes and polysomes. Incubation in high salt concentrations (0.8 M KCl) suggested that the affinity of Sal4p for the 40S subunit was lower than that for monosomes or polysomes. The Sal4p:ribosome association was only maintained when ribosomes were prepared in the presence of the translation elongation inhibitor cycloheximide; in uninhibited cells much lower levels of Sal4p were detectable in the 'run-off' polysomes. In view of these data, and given the stoichiometry of Sal4p to individual ribosomal proteins (estimated at less than 1:20), we suggest that Sal4p plays an ancillary role in translation termination.

Changes in the dosage of genes encoding elongation factor EF-la were shown to cause parallel changes in the misreading of nonsense codons. Higher amounts of EF-la were correlated with increased nonsense suppression, suggesting that the level of EF-la is critically involved in translational fidelity.To understand how translational accuracy is controlled, it is important to identify which genes are involved and to determine how they exert their effects. The best-studied mutations that alter translational fidelity in yeast cells are the codon-specific suppressors caused by altered tRNA anticodons (for reviews, see references 32 and 40). Among other genes that affect translational accuracy are the omnipotent suppressors, e.g., sup35 and sup45, which cause non-codonspecific misreading (3,9,11,17, 42), and the recessive antisuppressor, asu9, which increases translational fidelity in sup35 and sup45 strains (19,20). While attempting to clone asu9, we found that an extra copy of one of two redundant genes coding for the translation elongation factor EF-la increased suppression efficiency in a sup45-2 asu9 strain.EF-la is an important component of the translational apparatus. It promotes the GTP-dependent binding of aminoacyl-tRNA to the ribosome and participates in the proofreading of the codon-anticodon match (16,23,38). Yeast EF-la is encoded by two unlinked genes, TEF1 and TEF2 (5,25,26,31). The two genes are efficiently transcribed at about the same level, and the presence of either gene is sufficient for cell viability and normal growth rates (4). Mutations in the yeast EF-la and its Escherichia coli analog EF-Tu have been found to affect translational fidelity (13,14,30,37,41). In yeast cells, single mutational changes in TEF2 were shown to cause dominant suppression of both nonsense and frameshift mutations (30). In this paper, we show that the level of EF-la also affects translational fidelity.(Preliminary accounts of some of these results have been reported elsewhere [J. M. Song and S. W. Liebman, Yeast 2:S364, 1986; S. W. Liebman, J. M. Song, J. All-Robyn, E. Griffin, and D. Kelley-Geraghty, NATO ASI Ser. H14: [403][404][405][406][407][408][409][410][411][412][413][414] 1988].)A DNA clone containing the TEF1 gene complements asu9. Saccharomyces cerevisiae strain SL680-4B (a asu9-1 sup45-2 leu2-1 met8-1 trpl-1 ade3-26 hisS-2 lys2-1 canl-132 ura3-52) was chosen as the host for selection of asu9 complementing clones. In this strain, the asu9-1 mutation prevented growth on medium containing trichodermin (0.5 ,ug/ml; kindly provided by Leo Pharmaceutical Products), and the asu9-1 and sup45-2 mutations together permitted only a low * Corresponding author. and replated on medium with uracil, leucine, and methionine omitted and containing 0.5 jxg of trichodermin per ml to select for asu9 complementing clones. Plasmid pJS7, isolated from one of the fastest-growing transformants on this medium, caused both a slight reduction in the trichodermin sensitivity and enhanced suppression of leu2-1 and met8-1 upon retransformat...

Fisheries encompass complex interplays between social, economic, and environmental factors, but limitations on historical fisheries data can hamper efforts to identify and contextualize the long-term spatiotemporal patterns that shape them. We integrate 2500 years of stable isotope (δ34S, δ13C, and δ15N) and zooarchaeological evidence from Gulf of Mexico fisheries to assess cultural, demographic, and technological changes affecting sheepshead (Archosargus probatocephalus) populations and fishing practices in Louisiana, USA. Concurrent with human population growth, average sizes of sheepshead caught decreased from the 1720s to 1830s. The size of fish caught after the 1830s increased to pre-1720 levels at the same time that isotopic compositions of fish bone collagen show that fish were being caught from a more diverse range of ecosystems, including distant seagrass beds. Our findings provide the first evidence for large-scale depressions of historical sheepshead populations and the processes driving them, including rapid human population growth and sustained harvesting pressure.

Changes in the dosage of genes encoding elongation factor EF-1 alpha were shown to cause parallel changes in the misreading of nonsense codons. Higher amounts of EF-1 alpha were correlated with increased nonsense suppression, suggesting that the level of EF-1 alpha is critically involved in translational fidelity.