ArticleJournal of bacteriology2008
Twitching motility is essential for virulence in Dichelobacter nodosus.
Article in Journal of bacteriology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 62 citations in OpenAlex.
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- The role of PilU in the surface behaviors ofmLife · 2025Article
- Factors associated with ovine footrot lesions in Uruguayan flocks: a cross-sectional study.Frontiers in veterinary science · 2025Article
- Building permits-control of type IV pilus assembly by PilB and its cofactors.Journal of bacteriology · 2024Review
- Cryo-EM structure of an extracellular Geobacter OmcE cytochrome filament reveals tetrahaem packing.Nature microbiology · 2022Article
- A type IVB pilin influences twitching motility andMicrobiology (Reading, England) · 2022Article
- Type IV pilus retraction enables sustained bacteremia and plays a key role in the outcome of meningococcal sepsis in a humanized mouse model.PLoS pathogens · 2021Article
- The type IV pilus protein PilU functions as a PilT-dependent retraction ATPase.PLoS genetics · 2019Article
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- Site-specific His/Asp phosphoproteomic analysis of prokaryotes reveals putative targets for drug resistance.BMC microbiology · 2017Article
- Shearing and Enrichment of Extracellular Type IV Pili.Methods in molecular biology (Clifton, N.J.) · 2017Article
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- Bacterial stigmergy: an organising principle of multicellular collective behaviours of bacteria.Scientifica · 2015Review
- Comparative analysis of surface-exposed virulence factors of Acinetobacter baumannii.BMC genomics · 2014Article
- Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type IV fimbriae are essential virulence factors of Dichelobacter nodosus, the principal causative agent of ovine foot rot. The fimA fimbrial subunit gene is required for virulence, but fimA mutants exhibit several phenotypic changes and it is not certain if the effects on virulence result from the loss of type IV fimbria-mediated twitching motility, cell adherence, or reduced protease secretion. We showed that mutation of either the pilT or pilU gene eliminated the ability to carry out twitching motility. However, the pilT mutants displayed decreased adhesion to epithelial cells and reduced protease secretion, whereas the pilU mutants had wild-type levels of extracellular protease secretion and adherence. These data provided evidence that PilT is required for the type IV fimbria-dependent protease secretion pathway in D. nodosus. It was postulated that sufficient fimbrial retraction must occur in the pilU mutants to allow protease secretion, but not twitching motility, to take place. Although no cell movement was detected in a pilU mutant of D. nodosus, aberrant motion was detected in an equivalent mutant of Pseudomonas aeruginosa. These observations explain how in D. nodosus protease secretion can occur in a pilU mutant but not in a pilT mutant. In addition, virulence studies with sheep showed that both the pilT and pilU mutants were avirulent, providing evidence that mutation of the type IV fimbrial system affects virulence by eliminating twitching motility, not by altering cell adherence or protease secretion.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.