ArticlePLoS pathogens2023
SPI-1 virulence gene expression modulates motility of Salmonella Typhimurium in a proton motive force- and adhesins-dependent manner.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed.
- Molecular strategies ofFrontiers in cellular and infection microbiology · 2026Review
- Epidemiology, resistance profiles, and molecular characteristics of pediatric salmonella isolates: prevalence of a clonalFrontiers in cellular and infection microbiology · 2026Article
- Dose-dependent effects of dietary quercetin on cecal microbiota, hematological responses, and production efficiency in Arbor Acres broiler chickens.Veterinary world · 2026Article
- Salmonellosis as a One Health-One Biofilm Challenge: Biofilm Formation byPharmaceuticals (Basel, Switzerland) · 2025Review
- Deciphering the role of SsaE in biofilm regulation and T3SS-dependent virulence of Salmonella Typhimurium.World journal of microbiology & biotechnology · 2025Article
- Intracellular formate modulates a motility-invasion switch in Salmonella Typhimurium.PLoS pathogens · 2025Article
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- Nanovibrational Stimulation ofACS nano · 2024Article
- T3SS protein EsrC binds to theApplied and environmental microbiology · 2024Article
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9 authors.
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Abstract
Both the bacterial flagellum and the evolutionary related injectisome encoded on the Salmonella pathogenicity island 1 (SPI-1) play crucial roles during the infection cycle of Salmonella species. The interplay of both is highlighted by the complex cross-regulation that includes transcriptional control of the flagellar master regulatory operon flhDC by HilD, the master regulator of SPI-1 gene expression. Contrary to the HilD-dependent activation of flagellar gene expression, we report here that activation of HilD resulted in a dramatic loss of motility, which was dependent on the presence of SPI-1. Single cell analyses revealed that HilD-activation triggers a SPI-1-dependent induction of the stringent response and a substantial decrease in proton motive force (PMF), while flagellation remains unaffected. We further found that HilD activation enhances the adhesion of Salmonella to epithelial cells. A transcriptome analysis revealed a simultaneous upregulation of several adhesin systems, which, when overproduced, phenocopied the HilD-induced motility defect. We propose a model where the SPI-1-dependent depletion of the PMF and the upregulation of adhesins upon HilD-activation enable flagellated Salmonella to rapidly modulate their motility during infection, thereby enabling efficient adhesion to host cells and delivery of effector proteins.
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