This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hasselbring, B. M.
Right arrow Articles by Krause, D. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hasselbring, B. M.
Right arrow Articles by Krause, D. C.

 Previous Article  |  Next Article 

Journal of Bacteriology, October 2007, p. 7442-7449, Vol. 189, No. 20
0021-9193/07/$08.00+0     doi:10.1128/JB.00867-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Proteins P24 and P41 Function in the Regulation of Terminal-Organelle Development and Gliding Motility in Mycoplasma pneumoniae{triangledown}

Benjamin M. Hasselbring and Duncan C. Krause*

Department of Microbiology, University of Georgia, Athens, Georgia 30602

Received 4 June 2007/ Accepted 2 August 2007

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.

* Corresponding author. Mailing address: Department of Microbiology, 019 Riverbend South, 220 Riverbend Road, University of Georgia, Athens, GA 30602. Phone: (706) 542-2671. Fax: (706) 542-3804. E-mail: dkrause{at}uga.edu

{triangledown} Published ahead of print on 10 August 2007.

Journal of Bacteriology, October 2007, p. 7442-7449, Vol. 189, No. 20
0021-9193/07/$08.00+0     doi:10.1128/JB.00867-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»