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doi:10.1534/genetics.106.069906
A more recent version of this article appeared on May 1, 2007.
REGULAR RESEARCH PAPERS |
Adaptive divergence in experimental populations of Pseudomonas fluorescens. III. Mutational origins of wrinkly spreader diversity
Eleni Bantinaki 1, Rees Kassen 2, Christopher Knight 3, Zena Robinson 1, Andrew Spiers 4 and Paul Rainey 5*
1 University of Oxford
2 University of Ottawa
3 University of Manchester
4 Centre for Ecology and Hydrology, Oxford
5 University of Auckland
* To whom correspondence should be addressed. E-mail: p.rainey{at}auckland.ac.nz.
Submitted on December 17, 2006
Revised on February 13, 2007
Accepted on 19 February 2007
Understanding the connection between 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 showed that regulation and function of Wsp is analogous to the Che chemotaxis pathway from E. coli. Of significance is the methyl transferase (WspC) and methyl esterase (WspF) whose opposing activities form an integral feedback loop that controls the activity of the kinase (WspE). Logical deductions based on the regulatory model suggested that mutations within wspF were a likely cause of WS - a prediction that proved correct. 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.
Key Words: chemotaxis, mutational effects, signal transduction
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