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Originally published as Genetics Published Articles Ahead of Print on March 4, 2007.

Genetics, Vol. 176, 441-453, May 2007, Copyright © 2007
doi:10.1534/genetics.106.069906

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Adaptive Divergence in Experimental Populations of Pseudomonas fluorescens. III. Mutational Origins of Wrinkly Spreader Diversity

Eleni Bantinaki, Rees Kassen1, Christopher G. Knight2, Zena Robinson, Andrew J. Spiers and Paul B. Rainey3

Department of Plant Sciences, University of Oxford, Oxford OX1 3RB, United Kingdom

3 Corresponding author: School of Biological Sciences, University of Auckland, Private Bag 92019, Auckland 1001, New Zealand.
E-mail: p.rainey{at}auckland.ac.nz

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.




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