EC Number   |
General Information |
Reference |
|---|
  5.4.99.45 | malfunction |
deletion of the PUS3 gene has an effect on the efficiency of the translation process. Reduced readthrough efficiency of each stop codon by natural nonsense suppressor tRNAs |
648865 |
| 5.4.99.45 | malfunction |
disruption of the DEG1 gene is not lethal but reduces considerably the yeast growth rate, especially at an elevated temperature, 37 °C |
648860 |
| 5.4.99.45 | malfunction |
loss of Deg1/Pus3 and concomitant elimination of pseudouridine in tRNA at positions 38 and 39 (Psi38/39) specifically impairs the function of tRNAGln UUG under conditions of temperature-induced downregulation of wobble uridine thiolation in budding yeast. In the tRNATyr GPspiA variant SUP4, UAA read-through is enabled due to an anticodon mutation (UPsiA), whereas sup70-65 is a mutant form of tRNAGln CUG (SUP70) that mediates UAG decoding due to a mutation of the anticodon-loop closing base pair (G31:C39 to A31:C39). While SUP4 function is unaltered in deg1/pus3 mutants, the ability of sup70-65 to mediate non-sense suppression and to complement a genomic deletion of the essential SUP70 gene is severely compromised. Differential suppression of growth defects in deg1 mutants by multi-copy SUP70 or tQ(UUG). Phenotypic effects of DEG1 deletion may be rescuable by overexpression of tRNAGln UUG, since this is the major Gln isoacceptor and consequently more important for overall translation as compared to the minor tRNAGln CUG |
-, 747244 |
| 5.4.99.45 | physiological function |
in yeast, Deg1 dependent formation of Psi occurs in a majority of tRNAs either at position 38 or 39. Psi38 is most important for tRNAGln UUG function under heat stress but becomes crucial for tRNAGln CUG as well when the anticodon loop is destabilized by the sup70-65 mutation. Thus, Psi38/39 may protect the anticodon loop configuration from disturbances by loss of other modifications or base changes. Deg1-mediated Psi39 in itself does not detectably impact on the function of SUP4 in non-sense suppression in two different read-through contexts. Role of Psi38/39 for non-sense suppression for SUP4 or SUP70-65 |
-, 747244 |
| 5.4.99.45 | physiological function |
Pus3p is unique in its ability to modulate frameshifting and readthrough events during translation. This aspect of its activity may be responsible for HOT1 recombination phenotypes observed in deg1 mutants |
713040 |
