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TusDCB, a sulfur transferase complex involved in tRNA modification, contributes to UPEC pathogenicity.
Yumika Sato1, Ayako Takita1, Kazutomo Suzue2
1Department of Bacteriology, Graduate School of Medicine, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma, 371-8511, Japan.
Scientific Reports
|April 18, 2024
Summary
The TusDCB protein complex is vital for uropathogenic E. coli (UPEC) virulence, essential for producing virulence factors and causing urinary tract infections. Its sulfur transfer activity is critical for UPEC pathogenicity, offering a potential therapeutic target.
Area of Science:
- Microbiology
- Molecular Biology
- Biochemistry
Background:
- Transfer RNA (tRNA) modifications are crucial for accurate protein synthesis and cellular homeostasis in eukaryotes.
- The physiological roles of tRNA modifications, especially sulfur modifications, in bacterial pathogenesis are not well understood.
- The TusDCB protein complex, involved in tRNA sulfur modification, is conserved in γ-proteobacteria, including Escherichia coli.
Purpose of the Study:
- To investigate the role of the TusDCB protein complex in the virulence of uropathogenic Escherichia coli (UPEC).
- To determine the contribution of TusDCB's sulfur transfer activity to UPEC pathogenicity.
- To explore TusDCB as a potential therapeutic target against multidrug-resistant UPEC strains.
Main Methods:
- Generating deletion mutants of the tusDCB gene in UPEC.
- Assessing the impact of tusDCB deletion on the production of virulence factors like type 1 fimbriae and flagellum.
- Evaluating the virulence of UPEC strains in a mouse model of urinary tract infection.
- Analyzing the role of sulfur transfer activity using mutants with impaired sulfur transfer and related genes (tusE, mnmA).
Main Results:
- TusDCB is essential for the optimal production of UPEC virulence factors, including type 1 fimbriae and flagellum.
- Deletion of tusDCB significantly reduced UPEC's ability to aggregate in bladder epithelial cells and decreased virulence in a mouse model.
- TusDCB's sulfur transfer activity is indispensable for UPEC pathogenicity, as demonstrated by studies on sulfur-deficient mutants.
- tusDCB deletion attenuated virulence in highly pathogenic, multidrug-resistant UPEC strains.
Conclusions:
- The TusDCB protein complex and its tRNA sulfur modification activity are critical for UPEC virulence.
- TusDCB influences bacterial aggregation and the expression of key virulence factors.
- Targeting TusDCB presents a promising strategy for developing novel therapeutics against UPEC, including drug-resistant strains.
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