ArticleJournal of bacteriology2012
P65 truncation impacts P30 dynamics during Mycoplasma pneumoniae gliding.
Article in Journal of bacteriology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed.
- Immune dysregulation inFrontiers in immunology · 2026Review
- 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
- Reviewing advancement inFrontiers in microbiology · 2024Review
- Widespread ribosome stalling in a genome-reduced bacterium and the need for translational quality control.iScience · 2021Article
- Review
- Immunodominant proteins P1 and P40/P90 from human pathogen Mycoplasma pneumoniae.Nature communications · 2020Article
- Behaviors and Energy Source ofJournal of bacteriology · 2019Article
- Sialylated Receptor Setting Influences Mycoplasma pneumoniae Attachment and Gliding Motility.Molecular microbiology · 2018Article
- Mycoplasma pneumoniae from the Respiratory Tract and Beyond.Clinical microbiology reviews · 2017Review
- Integrated Information and Prospects for Gliding Mechanism of the Pathogenic Bacterium Mycoplasma pneumoniae.Frontiers in microbiology · 2016Article
- Potential Molecular Targets for Narrow-Spectrum Agents to Combat Mycoplasma pneumoniae Infection and Disease.Frontiers in microbiology · 2016Review
- Systematic Structural Analyses of Attachment Organelle in Mycoplasma pneumoniae.PLoS pathogens · 2015Article
- 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
- Protein kinase/phosphatase function correlates with gliding motility in Mycoplasma pneumoniae.Journal of bacteriology · 2013Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The cell wall-less prokaryote Mycoplasma pneumoniae is a major cause of community-acquired bronchitis and pneumonia in humans. Colonization is mediated largely by a differentiated terminal organelle, which is also the leading end in gliding motility. Cytadherence-associated proteins P30 and P65 appear to traffic concurrently to the distal end of developing terminal organelles. Here, truncation of P65 due to transposon insertion in the corresponding gene resulted in lower gliding velocity, reduced cytadherence, and decreased steady-state levels of several terminal organelle proteins, including P30. Utilizing fluorescent protein fusions, we followed terminal organelle development over time. New P30 foci appeared at nascent terminal organelles in P65 mutants, as in the wild type. However, with forward cell motility, P30 in the P65 mutants appeared to drag toward the trailing cell pole, where it was released, yielding a fluorescent trail to which truncated P65 colocalized. In contrast, P30 was only rarely observed at the trailing end of gliding wild-type cells. Complementation with the recombinant wild-type P65 allele by transposon delivery restored P65 levels and stabilized P30 localization to the terminal organelle.
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Registered trials
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