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Fruchard, L.

Publications and source records attributed to Fruchard, L..

3 recordsLinked to original sources

The tRNA epitranscriptomic landscape and RNA modification enzymes in Vibrio cholerae

Transfer RNAs (tRNAs) are central to protein synthesis, ensuring precise decoding of the genetic code by delivering aminoacids to the ribosome. Among all RNA species, tRNAs are the most heavily and diversely modified, with modifications playing critical roles in stability, folding, and function. Here, we present a comprehensive, isodecoder-level map of tRNA modifications in the human pathogen Vibrio cholerae. This map was generated by chemical-based sequencing methods, comparing wild-type and deletion strains. By assigning specific tRNA modifications to their cognate enzymes, we defined a comprehensive modification landscape in Vibrio cholerae and confirmed species-specific features, such as the presence of a functional TrmK enzyme, largely restricted to Gram-positive bacteria. Additionally, we detected a modification at U55 that occurs independently of TruB. To assess the biological significance of these modifications, we evaluated fitness under both standard conditions and subinhibitory antibiotic stress, and examined how modifications in the anticodon stem-loop region influence codon decoding efficiency and accuracy. Based on a comparative analysis of E. coli and V. cholerae, we discuss how species-specific differences in tRNA isodecoder gene repertoires may influence the functional impact and biological importance of tRNA modifications. This work provides the first experimentally validated, genome-wide map of tRNA modifications in V. cholerae, serving as a reference for future research into RNA modifications, translation regulation, and pathogen biology. Author summaryThis study charts the first genome-wide map of transfer RNA (tRNA) modifications in the cholera pathogen, Vibrio cholerae, revealing how chemical marks on tRNAs shape translation and stress responses. Using complementary chemical sequencing methods and a panel of targeted gene deletions, we assigned specific modifications to their enzymes across individual tRNA isodecoders. This integrative approach validates conserved features (e.g., {Psi}55 and T54), and specific ones, such as an active TrmK that installs m{superscript 1}A22 despite being considered largely restricted to Gram-positive bacteria, and uncovers enzyme interplay among dihydrouridine synthases. By testing mutant strains in standard and sub-inhibitory antibiotic conditions, we show that several modifications are dispensable for basal growth but become critical under proteotoxic stress, influencing fitness and translation accuracy, including stop-codon readthrough. Codon-specific reporter assays further demonstrate that modifications at wobble position 34 and at position 37 modulate decoding of distinct codon families, linking epitranscriptomic changes to gene expression programs. Comparative analysis with Escherichia coli suggests that species-specific tRNA isodecoder repertoires tune the functional impact of modifications. Our map provides an additional reference for studying RNA modification biology in pathogens and how it contributes to stress adaptation and virulence.

microbiology↗

Queuosine modification of tRNA-Tyrosine elicits translational reprogramming and enhances growth of Vibrio cholerae with aminoglycosides.

Tgt is the enzyme modifying the guanine (G) in tRNAs with GUN anticodon to queuosine (Q). tgt is required for optimal growth of Vibrio cholerae in the presence of sub-lethal aminoglycoside concentrations. We further explored here the role of the Q34 in the efficiency of codon decoding upon tobramycin exposure. We characterized its impact on the overall bacterial proteome, and elucidated the molecular mechanisms underlying the effects of Q34 modification in antibiotic translational stress response. Using molecular reporters, we showed that Q34 impacts the efficiency of decoding at tyrosine TAT and TAC codons. Proteomics analyses revealed that the anti-SoxR factor RsxA is better translated in the absence of tgt. RsxA displays a codon bias towards tyrosine TAT and overabundance of RsxA leads to decreased expression of genes belonging to SoxR oxidative stress regulon. We also identified conditions that regulate tgt expression. We propose that regulation of Q34 modification in response to environmental cues leads to translational reprogramming of transcripts bearing a biased tyrosine codon usage. In silico analysis further identified candidate genes which could be subject to such translational regulation, among which DNA repair factors. Such transcripts, fitting the definition of modification tunable transcripts, are central in the bacterial response to antibiotics.

microbiology↗

Non-essential tRNA and rRNA modifications impact the bacterial response to sub-MIC antibiotic stress

Antimicrobial resistance (AMR) develops as a major problem in infectious diseases treatment. While antibiotic resistance mechanisms are usually studied using lethal antibiotic doses, lower doses allowing bacterial growth are now considered as factors influencing the development and selection of resistance. Based on high throughput transposon insertion sequencing (TN-seq) in V. cholerae, we have undertaken the phenotypic characterization of 23 transfer RNA (tRNA) and ribosomal RNA (rRNA) modifications deletion mutants, for which growth is globally not affected in the absence of stress. We uncover a specific involvement of different RNA modification genes in the response to aminoglycosides (tobramycin (TOB), gentamicin (GEN)), fluoroquinolones (ciprofloxacin (CIP)), {beta}-lactams (carbenicillin (CRB)), chloramphenicol (CM) and trimethoprim (TRM). Our results identify t/rRNA modification genes, not previously associated to any antibiotic resistance phenotype, as important factors affecting the bacterial response to sub-MIC antibiotics from different families. This suggests differential translation and codon decoding as critical factors involved in the bacterial response to stress.

microbiology↗