ArticleJournal of bacteriology2005
Mutant analysis reveals a specific requirement for protein P30 in Mycoplasma pneumoniae gliding motility.
Article in Journal of bacteriology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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Who cites it
33 citing papers in PubMed, 57 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
- Advances in adhesion-related pathogenesis inFrontiers in microbiology · 2025Review
- Reviewing advancement inFrontiers in microbiology · 2024Review
- Force and Stepwise Movements of Gliding Motility in Human Pathogenic BacteriumFrontiers in microbiology · 2021Article
- Distinct Mycoplasma pneumoniae Interactions with Sulfated and Sialylated Receptors.Infection and immunity · 2020Article
- Sialylated Receptor Setting Influences Mycoplasma pneumoniae Attachment and Gliding Motility.Molecular microbiology · 2018Article
- Electron cryotomography of Mycoplasma pneumoniae mutants correlates terminal organelle architectural features and function.Molecular microbiology · 2018Article
- VARIABLE SELECTION AND BIOMARKER CORRELATION IN THE ANALYSIS OFAnalytical letters · 2017Article
- Article
- 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
- 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
- Mycoplasma pulmonis Vsa proteins and polysaccharide modulate adherence to pulmonary epithelial cells.FEMS microbiology letters · 2012Article
- P65 truncation impacts P30 dynamics during Mycoplasma pneumoniae gliding.Journal of bacteriology · 2012Article
- Vaccination of BALB/c mice with an avirulent Mycoplasma pneumoniae P30 mutant results in disease exacerbation upon challenge with a virulent strain.Infection and immunity · 2012Article
- Processing is required for a fully functional protein P30 in Mycoplasma pneumoniae gliding and cytadherence.Journal of bacteriology · 2011Article
- Insights into the function of Mycoplasma pneumoniae protein P30 from orthologous gene replacement.Microbiology (Reading, England) · 2011Article
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, long considered among the smallest and simplest cells capable of self-replication, has a distinct cellular polarity characterized by the presence of a differentiated terminal organelle which functions in adherence to human respiratory epithelium, gliding motility, and cell division. Characterization of hemadsorption (HA)-negative mutants has resulted in identification of several terminal organelle proteins, including P30, the loss of which results in developmental defects and decreased adherence to host cells, but their impact on M. pneumoniae gliding has not been investigated. Here we examined the contribution of P30 to gliding motility on the basis of satellite growth and cell gliding velocity and frequency. M. pneumoniae HA mutant II-3 lacking P30 was nonmotile, but HA mutant II-7 producing a truncated P30 was motile, albeit at a velocity 50-fold less than that of the wild type. HA-positive revertant II-3R producing an altered P30 was unexpectedly not fully wild type with respect to gliding. Complementation of mutant II-3 with recombinant wild-type and mutant alleles confirmed the correlation between gliding defect and loss or alteration in P30. Surprisingly, fusion of yellow fluorescent protein to the C terminus of P30 had little impact on cell gliding velocity and significantly enhanced HA. Finally, while quantitative examination of HA revealed clear distinctions among these mutant strains, gliding defects did not correlate strictly with the HA phenotype, and all strains attached to glass at wild-type levels. Taken together, these findings suggest a role for P30 in gliding motility that is distinct from its requirement in adherence.
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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.