Microbiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Microbiology 155 (2009), 1080-1092; DOI  10.1099/mic.0.024661-0IMMEDIATE OPEN ACCESS ARTICLE
This Article
Free via Open Access: OA
Right arrow OA Free Full Text
Right arrow Full Text (PDF)
Right arrow Supplementary material
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
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 arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bartosik, A. A.
Right arrow Articles by Jagura-Burdzy, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bartosik, A. A.
Right arrow Articles by Jagura-Burdzy, G.
Agricola
Right arrow Articles by Bartosik, A. A.
Right arrow Articles by Jagura-Burdzy, G.
Microbiology 155 (2009), 1080-1092; DOI  10.1099/mic.0.024661-0
© 2009 Society for General Microbiology

ParB deficiency in Pseudomonas aeruginosa destabilizes the partner protein ParA and affects a variety of physiological parameters

A. A. Bartosik1, J. Mierzejewska1, C. M. Thomas2 and G. Jagura-Burdzy1

1 Institute of Biochemistry and Biophysics, PAS, 02-106 Warsaw, Pawinskiego 5A, Poland
2 School of Biosciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

Correspondence
G. Jagura-Burdzy
gjburdzy{at}ibb.waw.pl

Deletions leading to complete or partial removal of ParB were introduced into the Pseudomonas aeruginosa chromosome. Fluorescence microscopy of fixed cells showed that ParB mutants lacking the C-terminal domain or HTH motif formed multiple, less intense foci scattered irregularly, in contrast to the one to four ParB foci per cell symmetrically distributed in wild-type P. aeruginosa. All parB mutations affected both bacterial growth and swarming and swimming motilities, and increased the production of anucleate cells. Similar effects were observed after inactivation of parA of P. aeruginosa. As complete loss of ParA destabilized its partner ParB it was unclear deficiency of which protein is responsible for the mutant phenotypes. Analysis of four parB mutants showed that complete loss of ParB destabilized ParA whereas three mutants that retained the N-terminal 90 aa of ParB did not. As all four parB mutants demonstrate the same defects it can be concluded that either ParB, or ParA and ParB in combination, plays an important role in nucleoid distribution, growth and motility in P. aeruginosa.

Abbreviations: DAPI, 4',6-diamidino-2-phenylindole

Supplementary methods and three supplementary figures are available with the online version of this paper.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 2009 Society for General Microbiology.