QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Supplemental Research Data Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Radhakrishnan, S. K. Articles by Viollier, P. H. Search for Related Content PubMed PubMed Citation Articles by Radhakrishnan, S. K. Articles by Viollier, P. H. Social Bookmarking                   What's this?

The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus

¹ Department of Molecular Biology and Microbiology, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA; ² Max Planck Institute for Terrestrial Microbiology, D-35043 Marburg, Germany

Caulobacter crescentus divides asymmetrically into a swarmer cell and a stalked cell, a process that is governed by the imbalance in phosphorylated levels of the DivK cell fate determinant in the two cellular compartments. The asymmetric polar localization of the DivJ kinase results in its specific inheritance in the stalked daughter cell where it phosphorylates DivK. The mechanism for the polar positioning of DivJ is poorly understood. SpmX, an uncharacterized lysozyme homolog, is shown here to control DivJ localization and activation. In the absence of SpmX, DivJ is delocalized and dysfunctional, resulting in developmental defects caused by an insufficiency in phospho-DivK. While SpmX stimulates DivK phosphorylation in the stalked cell, unphosphorylated DivK in the swarmer cell activates an intricate transcriptional cascade that leads to the production of the spmX message. This event primes the swarmer cell for the impending transition into a stalked cell, a transition that is sparked by the abrupt accumulation and localization of SpmX to the future stalked cell pole. Localized SpmX then recruits and stimulates DivJ, and the resulting phospho-DivK implements the stalked cell fate. The dynamic interplay between SpmX and DivK is at the heart of the molecular circuitry that sustains the Caulobacter developmental cycle.

[Keywords: Asymmetric cell division; cell fate determinant; polar protein localization; muramidase; kinase]]

Received August 6, 2007; revised version accepted November 21, 2007.

E-MAIL patrick.viollier{at}case.edu; FAX (216) 368-1055.

Supplemental material is available at http://www.genesdev.org.

Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.1601808

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?