A bacterial tRNA gene set rapidly evolves, compensating the loss of one tRNA type by large duplication events that increase the gene copy number of a second, different tRNA type.

Experimental evolution and systematic sequence analysis of transfer RNA genes reveal that anticodon mutations provide adaptive plasticity to the translation machinery.

Biochemical and genome-wide analysis demonstrates that m¹G37 is important for tRNA aminoacylation and for the entire elongation cycle of protein synthesis.

Manipulation of the E. coli translation machinery sheds new light on evolutionary constraints and optimization strategies for bacterial translation and growth.

The role of an amino acid-dependent tRNA modification as a nutrient sensor and regulator of metabolic homeostasis has been discovered.

Systematic CRISPR-based editing of tRNA genes revealed that different human cells that span a range of growth rates and different modes of proliferation states require diverse tRNA sets.

Surveying Mycobacterium tuberculosis tRNA modification leads to identification of a modification promoting Mtb pathogenesis.

Genomic-profiles and reporters reveal that the three-nucleotide ‘words’ read by the ribosome, codons, have a strong effect on mRNA stability, impacting the homeostatic mRNA and protein levels in human cells.

The transfer RNA thiolation modification is required for the efficient translation of the master immune regulator NPR1 in plants.

A parsimonious biophysical model correctly predicts the conserved expression stoichiometry of core bacterial mRNA translation factors, providing intuitive and quantitative design principles for in vivo pathway construction.