ArticleJournal of bacteriology1999
Identification and complementation of frameshift mutations associated with loss of cytadherence in Mycoplasma pneumoniae.
Article in Journal of bacteriology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Assembly Formation of P65 Protein, Featured by an Intrinsically Disordered Region Involved in Gliding Machinery ofBiomolecules · 2025Article
- Molecular ruler of the attachment organelle in Mycoplasma pneumoniae.PLoS pathogens · 2021Article
- Systematic Structural Analyses of Attachment Organelle in Mycoplasma pneumoniae.PLoS pathogens · 2015Article
- Protein kinase/phosphatase function correlates with gliding motility in Mycoplasma pneumoniae.Journal of bacteriology · 2013Article
- P65 truncation impacts P30 dynamics during Mycoplasma pneumoniae gliding.Journal of bacteriology · 2012Article
- Processing is required for a fully functional protein P30 in Mycoplasma pneumoniae gliding and cytadherence.Journal of bacteriology · 2011Article
- Domain analysis of protein P30 in Mycoplasma pneumoniae cytadherence and gliding motility.Journal of bacteriology · 2011Article
- Mycoplasma pneumoniae cytoskeletal protein HMW2 and the architecture of the terminal organelle.Journal of bacteriology · 2009Article
- Mycoplasma pneumoniae J-domain protein required for terminal organelle function.Molecular microbiology · 2009Article
- Phase-locked mutants of Mycoplasma agalactiae: defining the molecular switch of high-frequency Vpma antigenic variation.Molecular microbiology · 2008Article
- Proteins P24 and P41 function in the regulation of terminal-organelle development and gliding motility in Mycoplasma pneumoniae.Journal of bacteriology · 2007Article
- Protein P200 is dispensable for Mycoplasma pneumoniae hemadsorption but not gliding motility or colonization of differentiated bronchial epithelium.Infection and immunity · 2007Article
- Transposon mutagenesis identifies genes associated with Mycoplasma pneumoniae gliding motility.Journal of bacteriology · 2006Article
- Mutant analysis reveals a specific requirement for protein P30 in Mycoplasma pneumoniae gliding motility.Journal of bacteriology · 2005Article
- Identification and complementation of a mutation associated with loss of Mycoplasma pneumoniae virulence-specific proteins B and C.Journal of bacteriology · 2005Article
- HMW1 is required for stability and localization of HMW2 to the attachment organelle of Mycoplasma pneumoniae.Journal of bacteriology · 2004Article
- Attachment organelle formation represented by localization of cytadherence proteins and formation of the electron-dense core in wild-type and mutant strains of Mycoplasma pneumoniae.Journal of bacteriology · 2003Article
- The complete genomic sequence of Mycoplasma penetrans, an intracellular bacterial pathogen in humans.Nucleic acids research · 2002Article
- Characterization of a Mycoplasma pneumoniae hmw3 mutant: implications for attachment organelle assembly.Journal of bacteriology · 2002Article
- Stability and subcellular localization of cytadherence-associated protein P65 in Mycoplasma pneumoniae.Journal of bacteriology · 2001Article
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4 authors.
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Abstract
Mycoplasma pneumoniae cytadherence is mediated by a specialized, polar attachment organelle. Certain spontaneously arising cytadherence mutants (designated class I) lack HMW2, fail to localize the adhesin protein P1 to the attachment organelle, and exhibit accelerated turnover of proteins HMW1, HMW3, and P65. Insertional inactivation of hmw2 by Tn4001 results in a phenotype nearly identical to that of the class I mutants, suggesting that the latter may result from a defect in hmw2. In this study, the recombinant wild-type hmw2 allele successfully complemented a class I mutant when introduced by transposon delivery. Synthesis of recombinant HMW2 at wild-type levels resulted in reacquisition of hemadsorption and normal levels of HMW1, HMW3, and P65. Low-level production of HMW2 in some transformants resulted in only an intermediate capacity to hemadsorb. Furthermore, full restoration of HMW1 and P65, but not that of HMW3, was directly proportional to the amount of recombinant HMW2 produced, reflecting the importance of proper stoichiometry for certain cytadherence-associated proteins. The recombinant class I hmw2 allele did not restore cytadherence, consistent with a defect in hmw2 in this mutant. A frameshift was discovered in different oligoadenine tracts in hmw2 from two independent class I mutants. Finally, protein P28 is thought to be the product of internal translation initiation in hmw2. A transposon excision-deletion mutant produced a truncated HMW2 but no P28, consistent with this conclusion. However, this deletion mutant was hemadsorption positive, indicating that P28 may not be required for cytadherence.
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