ArticleJournal of bacteriology2007
Proteins P24 and P41 function in the regulation of terminal-organelle development and gliding motility in Mycoplasma pneumoniae.
Article in Journal of bacteriology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed.
- FtsZ contributes to cytoadhesion and interaction with host extracellular matrix components and plasminogen in Mycoplasma bovis.Veterinary research · 2025Article
- Unraveling the role of distinct cytoskeletal motility structures in Mycoplasma pneumoniae relatives.BMC microbiology · 2025Review
- Advances in adhesion-related pathogenesis inFrontiers in microbiology · 2025Review
- Review
- ExploringFrontiers in microbiology · 2020Review
- Electron cryotomography of Mycoplasma pneumoniae mutants correlates terminal organelle architectural features and function.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
- A Compendium for Mycoplasma pneumoniae.Frontiers in microbiology · 2016Review
- Article
- A major determinant for gliding motility in Mycoplasma genitalium: the interaction between the terminal organelle proteins MG200 and MG491.The Journal of biological chemistry · 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
- P65 truncation impacts P30 dynamics during Mycoplasma pneumoniae gliding.Journal of bacteriology · 2012Article
- Loss of co-chaperone TopJ impacts adhesin P1 presentation and terminal organelle maturation in Mycoplasma pneumoniae.Molecular microbiology · 2011Article
- Domain analysis of protein P30 in Mycoplasma pneumoniae cytadherence and gliding motility.Journal of bacteriology · 2011Article
- Targeted chromosomal knockouts in Mycoplasma pneumoniae.Applied and environmental microbiology · 2010Article
- Functional domain analysis of the Mycoplasma pneumoniae co-chaperone TopJ.Molecular microbiology · 2010Article
- P110 and P140 cytadherence-related proteins are negative effectors of terminal organelle duplication in Mycoplasma genitalium.PloS one · 2009Article
- Mycoplasma pneumoniae J-domain protein required for terminal organelle function.Molecular microbiology · 2009Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Mycoplasma pneumoniae is a major cause of bronchitis and atypical pneumonia in humans. This cell wall-less bacterium has a complex terminal organelle that functions in cytadherence and gliding motility. The gliding mechanism is unknown but is coordinated with terminal-organelle development during cell division. Disruption of M. pneumoniae open reading frame MPN311 results in loss of protein P41 and downstream gene product P24. P41 localizes to the base of the terminal organelle and is required to anchor the terminal organelle to the cell body, but during cell division, MPN311 insertion mutants also fail to properly regulate nascent terminal-organelle development spatially or gliding activity temporally. We measured gliding velocity and frequency and used fluorescent protein fusions and time-lapse imaging to assess the roles of P41 and P24 individually in terminal-organelle development and gliding function. P41 was necessary for normal gliding velocity and proper spatial positioning of new terminal organelles, while P24 was required for gliding frequency and new terminal-organelle formation at wild-type rates. However, P41 was essential for P24 function, and in the absence of P41, P24 exhibited a dynamic localization pattern. Finally, protein P28 requires P41 for stability, but analysis of a P28(-) mutant established that the MPN311 mutant phenotype was not a function of loss of P28.
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Registered trials
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