High impact information on KRS1

• GCN4 protein in turn stimulates transcription of GCD5, leading to increased LysRS activity [1].
• Autoregulation of the yeast lysyl-tRNA synthetase gene GCD5/KRS1 by translational and transcriptional control mechanisms [1].
• A mutation in the negative regulator GCD5 was isolated on the basis of its suppression of a gcn2 mutation [2].
• The effect of gcd5 is a posttranscriptional increase in histidine biosynthetic enzyme activity [2].
• The transcription initiation sites of the KRS1 gene were determined [3].

Biological context of KRS1

• The nucleotide sequence of a 3.6-kilobase pair DNA fragment containing the structural gene for yeast cytoplasmic lysyl-tRNA synthetase (KRS1) and its flanking regions was determined [3].
• A PMR2 tandem repeat with a modified C-terminus is located downstream from the KRS1 gene encoding lysyl-tRNA synthetase in Saccharomyces cerevisiae [4].
• Aminoacylation of tRNA(Pyl) transcript by a typical class II synthetase, LysRS from yeast, was possible when its amber anticodon CUA was mutated into a lysine UUU anticodon [5].

Anatomical context of KRS1

• All KRS1 derivatives were able to sustain growth of yeast cells, although the mutant cell lines displaying a low LysRS activity grew more slowly [6].

Other interactions of KRS1

• Complementation tests amongst the four new gcd-mutant strains, including strain RH558 gcd2-1 isolated earlier, yielded five complementation groups: GCD2, GCD3, GCD4, GCD5, and GCD6 [7].

References