Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow Print PDF (139K) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (4)
Right arrowRequest Permissions
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Siam, R.
Right arrow Articles by Marczynski, G. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Siam, R.
Right arrow Articles by Marczynski, G. T.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 2003, Vol. 31, No. 6 1775-1779
© 2003 Oxford University Press

Glutamate at the phosphorylation site of response regulator CtrA provides essential activities without increasing DNA binding

Rania Siam and Gregory T. Marczynski

Department of Microbiology and Immunology, McGill University, 3775 University Street, Montreal, Quebec H3A 2B4, Canada

*To whom correspondence should be addressed. Tel: +1 514 398 3917; Fax: +1 514 398 7052; Email: gmarczynski{at}microimm.mcgill.ca
Present address:
Rania Siam, The Salk Institute for Biological Sciences, Molecular and Cellular Biology Laboratory, 10010 N. Torrey Pines Road, La Jolla, CA 92037-1099, USA

The essential response regulator CtrA controls the Caulobacter crescentus cell cycle and phosphorylated CtrA~P preferentially binds target DNA in vitro. The CtrA aspartate to glutamate (D51E) mutation mimics phosphorylated CtrA~P in vivo and rescues non-viable C.crescentus cells. However, we observe that the CtrA D51E and the unphosphorylated CtrA wild-type proteins have identical DNA affinities and produce identical DNase I protection footprints inside the C.crescentus replication origin. There fore, D51E promotes essential CtrA activities separate from increased DNA binding. Accordingly, we argue that CtrA protein recruitment to target DNA is not sufficient to regulate cell cycle progression.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Bacteriol.Home page
S. Leonard, J. Ferooz, V. Haine, I. Danese, D. Fretin, A. Tibor, S. de Walque, X. De Bolle, and J.-J. Letesson
FtcR Is a New Master Regulator of the Flagellar System of Brucella melitensis 16M with Homologs in Rhizobiaceae
J. Bacteriol., January 1, 2007; 189(1): 131 - 141.
[Abstract] [Full Text] [PDF]

Home page
 GeneticsHome page
P. Goymer, S. G. Kahn, J. G. Malone, S. M. Gehrig, A. J. Spiers, and P. B. Rainey
Adaptive Divergence in Experimental Populations of Pseudomonas fluorescens. II. Role of the GGDEF Regulator WspR in Evolution and Development of the Wrinkly Spreader Phenotype
Genetics, June 1, 2006; 173(2): 515 - 526.
[Abstract] [Full Text] [PDF]

Home page
 J Mol EndocrinolHome page
K Boelaert, R Yu, L A Tannahill, A L Stratford, F L Khanim, M C Eggo, J S Moore, L S Young, N J L Gittoes, J A Franklyn, et al.
PTTG's C-terminal PXXP motifs modulate critical cellular processes in vitro
J. Mol. Endocrinol., December 1, 2004; 33(3): 663 - 677.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.