ArticleJournal of bacteriology2011
Domain analysis of protein P30 in Mycoplasma pneumoniae cytadherence and gliding motility.
Article in Journal of bacteriology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Unraveling the role of distinct cytoskeletal motility structures in Mycoplasma pneumoniae relatives.BMC microbiology · 2025Review
- Assembly Formation of P65 Protein, Featured by an Intrinsically Disordered Region Involved in Gliding Machinery ofBiomolecules · 2025Article
- The virome composition of respiratory tract changes in school-aged children with Mycoplasma pneumoniae infection.Virology journal · 2025Article
- Marine-Derived Sulfated Glycans Inhibit the Interaction of Heparin with Adhesion Proteins ofMarine drugs · 2024Article
- Reviewing advancement inFrontiers in microbiology · 2024Review
- Engineered live bacteria suppress Pseudomonas aeruginosa infection in mouse lung and dissolve endotracheal-tube biofilms.Nature biotechnology · 2023Article
- Pathogenicity and virulence ofVirulence · 2022Review
- Review
- Force and Stepwise Movements of Gliding Motility in Human Pathogenic BacteriumFrontiers in microbiology · 2021Article
- A Review ofFrontiers in veterinary science · 2021Review
- Immunodominant proteins P1 and P40/P90 from human pathogen Mycoplasma pneumoniae.Nature communications · 2020Article
- Mycoplasma pneumoniae from the Respiratory Tract and Beyond.Clinical microbiology reviews · 2017Review
- Insights into the pathogenesis of Mycoplasma pneumoniae (Review).Molecular medicine reports · 2016Review
- Potential Molecular Targets for Narrow-Spectrum Agents to Combat Mycoplasma pneumoniae Infection and Disease.Frontiers in microbiology · 2016Review
- Integrated Information and Prospects for Gliding Mechanism of the Pathogenic Bacterium Mycoplasma pneumoniae.Frontiers in microbiology · 2016Article
- Mycoplasma pneumoniae, an underutilized model for bacterial cell biology.Journal of bacteriology · 2014Review
- First identification of proteins involved in motility of Mycoplasma gallisepticum.Veterinary research · 2014Article
- In vitro spatial and temporal analysis of Mycoplasma pneumoniae colonization of human airway epithelium.Infection and immunity · 2014Article
- Effects of Traditional Chinese Medicine Qinbai Qingfei Concentrated Pellet on Cellular Infectivity of Mycoplasma pneumoniae.International scholarly research notices · 2014Article
- Molecular cloning and characterization of a surface-localized adhesion protein in Mycoplasma bovis Hubei-1 strain.PloS one · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The cell wall-less prokaryote Mycoplasma pneumoniae causes bronchitis and atypical pneumonia in humans. Mycoplasma attachment and gliding motility are required for colonization of the respiratory epithelium and are mediated largely by a differentiated terminal organelle. P30 is a membrane protein at the distal end of the terminal organelle and is required for cytadherence and gliding motility, but little is known about the functional role of its specific domains. In the current study, domain deletion and substitution derivatives of P30 were engineered and introduced into a P30 null mutant by transposon delivery to assess their ability to rescue P30 function. Domain deletions involving the extracellular region of P30 severely impacted protein stability and adherence and gliding function, as well as the capacity to stabilize terminal organelle protein P65. Amino acid substitutions in the transmembrane domain revealed specific residues uniquely required for P30 stability and function, perhaps to establish correct topography in the membrane for effective alignment with binding partners. Deletions within the predicted cytoplasmic domain did not affect P30 localization or its capacity to stabilize P65 but markedly impaired gliding motility and cytadherence. The larger of two cytoplasmic domain deletions also appeared to remove the P30 signal peptide processing site, suggesting a larger leader peptide than expected. We propose that the P30 cytoplasmic domain may be required to link P30 to the terminal organelle core, to enable the P30 extracellular domain to achieve a functional conformation, or perhaps both.
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Registered trials
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.