TusDCB, a sulfur transferase complex involved in tRNA modification, contributes to UPEC pathogenicity.
Bacterial pathogenesis
Biofilm
Drug resistance
Urinary tract infection (UTI)
Virulence
tRNA modification
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
18 Apr 2024
18 Apr 2024
Historique:
received:
19
12
2023
accepted:
12
04
2024
medline:
19
4
2024
pubmed:
19
4
2024
entrez:
18
4
2024
Statut:
epublish
Résumé
tRNA modifications play a crucial role in ensuring accurate codon recognition and optimizing translation levels. While the significance of these modifications in eukaryotic cells for maintaining cellular homeostasis and physiological functions is well-established, their physiological roles in bacterial cells, particularly in pathogenesis, remain relatively unexplored. The TusDCB protein complex, conserved in γ-proteobacteria like Escherichia coli, is involved in sulfur modification of specific tRNAs. This study focused on the role of TusDCB in the virulence of uropathogenic E. coli (UPEC), a bacterium causing urinary tract infections. The findings indicate that TusDCB is essential for optimal production of UPEC's virulence factors, including type 1 fimbriae and flagellum, impacting the bacterium's ability to aggregate in bladder epithelial cells. Deletion of tusDCB resulted in decreased virulence against urinary tract infection mice. Moreover, mutant TusDCB lacking sulfur transfer activity and tusE- and mnmA mutants revealed the indispensability of TusDCB's sulfur transfer activity for UPEC pathogenicity. The study extends its relevance to highly pathogenic, multidrug-resistant strains, where tusDCB deletion reduced virulence-associated bacterial aggregation. These insights not only deepen our understanding of the interplay between tRNA sulfur modification and bacterial pathogenesis but also highlight TusDCB as a potential therapeutic target against UPEC strains resistant to conventional antimicrobial agents.
Identifiants
pubmed: 38637685
doi: 10.1038/s41598-024-59614-2
pii: 10.1038/s41598-024-59614-2
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
8978Subventions
Organisme : Japan Society for the Promotion of Science
ID : 22H02864
Organisme : Japan Society for the Promotion of Science
ID : 22H02864
Organisme : Japan Society for the Promotion of Science
ID : 22H02864
Organisme : Japan Agency for Medical Research and Development
ID : 23gm1610013s0501
Organisme : Japan Agency for Medical Research and Development
ID : 22fk0108604h0901
Organisme : Health Labour Sciences Research Grant
ID : 21KA1004
Informations de copyright
© 2024. The Author(s).
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