Logo
 

Abertay Research Collections >
Research Centres >
SIMBIOS Collection >

Please use this identifier to cite or link to this item: http://hdl.handle.net/10373/673

View Statistics
Title: Adaptive divergence in experimental populations of Pseudomonas fluorescens. III. Mutational origins of wrinkly spreader diversity
Authors: Bantinaki, Eleni
Kassen, Rees
Knight, Christopher G.
Robinson, Zena
Spiers, Andrew J.
Rainey, Paul B.
Affiliation: University of Abertay Dundee. Scottish Informatics, Mathematics, Biology and Statistics Centre
Keywords: Pseudomonas fluorescens
Mutation
Adaptation
Issue Date: May-2007
Publisher: Genetics Society of America
Type: Journal Article
Refereed: peer-reviewed
Rights: Published version (c)Genetics Society of America, available from http://dx.doi.org/10.1534/genetics.106.069906
Citation: Bantinaki, E., et al. 2007. Adaptive divergence in experimental populations of Pseudomonas fluorescens. III. Mutational origins of wrinkly spreader diversity. Genetics. 176(1): pp.441-453. Available from http://dx.doi.org/10.1534/genetics.106.069906
Abstract: Understanding the connections among genotype, phenotype, and fitness through evolutionary time is a central goal of evolutionary genetics. Wrinkly spreader (WS) genotypes evolve repeatedly in model Pseudomonas populations and show substantial morphological and fitness differences. Previous work identified genes contributing to the evolutionary success of WS, in particular the di-guanylate cyclase response regulator, WspR. Here we scrutinize the Wsp signal transduction pathway of which WspR is the primary output component. The pathway has the hallmarks of a chemosensory pathway and genetic analyses show that regulation and function of Wsp is analogous to the Che chemotaxis pathway from Escherichia coli. Of significance is the methyltransferase (WspC) and methylesterase (WspF) whose opposing activities form an integral feedback loop that controls the activity of the kinase (WspE). Deductions based on the regulatory model suggested that mutations within wspF were a likely cause of WS. Analyses of independent WS genotypes revealed numerous simple mutations in this single open reading frame. Remarkably, different mutations have different phenotypic and fitness effects. We suggest that the negative feedback loop inherent in Wsp regulation allows the pathway to be tuned by mutation in a rheostat-like manner.
URI: http://hdl.handle.net/10373/673
ISSN: 0016-6731
Appears in Collections:SIMBIOS Collection

Files in This Item:

There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

 

Valid XHTML 1.0! DSpace Software Copyright © 2002-2010  Duraspace - Feedback