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Abstract

Pseudomonas fluorescens is a model for the study of adaptive radiation. When propagated in a spatially structured
environment, the bacterium rapidly diversifies into a range of niche specialist genotypes. Here we present a genetic dissection and
phenotypic characterization of the fuzzy spreader (FS) morphotype—a type that arises repeatedly during the course of the P. fluorescens
radiation and appears to colonize the bottom of static broth microcosms. The causal mutation is located within gene fuzY
(pflu0478)—the fourth gene of the five-gene fuzVWXYZ operon. fuzY encodes a b-glycosyltransferase that is predicted to modify
lipopolysaccharide (LPS) O antigens. The effect of the mutation is to cause cell flocculation. Analysis of 92 independent FS genotypes
showed each to have arisen as the result of a loss-of-function mutation in fuzY, although different mutations have subtly different
phenotypic and fitness effects. Mutations within fuzY were previously shown to suppress the phenotype of mat-forming wrinkly
spreader (WS) types. This prompted a reinvestigation of FS niche preference. Time-lapse photography showed that FS colonizes the
meniscus of broth microcosms, forming cellular rafts that, being too flimsy to form a mat, collapse to the vial bottom and then
repeatably reform only to collapse. This led to a reassessment of the ecology of the P. fluorescens radiation. Finally, we show that
ecological interactions between the three dominant emergent types (smooth, WS, and FS), combined with the interdependence of FS
and WS on fuzY, can, at least in part, underpin an evolutionary arms race with bacteriophage SBW25F2, to which mutation in fuzY
confers resistance.