TRNA methylation resolves codon usage bias at the limit of cell viability.

ABSTRACT: Codon usage of each genome is closely correlated with the abundance of tRNA isoacceptors. How codon usage bias is resolved by tRNA post-transcriptional modifications is largely unknown. Here we demonstrate that the N¹-methylation of guanosine at position 37 (m¹G37) on the 3'-side of the anticodon, while not directly responsible for reading of codons, is a neutralizer that resolves differential decoding of proline codons. A genome-wide suppressor screen of a non-viable Escherichia coli strain, lacking m¹G37, identifies proS suppressor mutations, indicating a coupling of methylation with tRNA prolyl-aminoacylation that sets the limit of cell viability. Using these suppressors, where prolyl-aminoacylation is decoupled from tRNA methylation, we show that m

SUBMITTER: Masuda I 

PROVIDER: S-EPMC9643105 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature