Abstract
The RpoS sigma factor protein of Escherichia coli RNA polymerase is the master transcriptional regulator of physiological responses to a variety of stresses. This stress response comes at the expense of scavenging for scarce resources, causing a trade-off between stress tolerance and nutrient acquisition. This trade-off favors non-functional rpoS alleles in nutrient-poor environments. We used experimental evolution to explore how natural selection modifies the regulatory network of strains lacking RpoS when they evolve in an osmotically stressful environment. We found that strains lacking RpoS adapt less variably, in terms of both fitness increase and changes in patterns of transcription, than strains with functional RpoS. This phenotypic uniformity was caused by the same adaptive mutation in every independent population: the insertion of IS10 into the promoter of the otsBA operon. OtsA and OtsB are required to synthesize the osmoprotectant trehalose, and transcription of otsBA requires RpoS in the wild-type genetic background. The evolved IS10 insertion rewires expression of otsBA from RpoS-dependent to RpoS-independent, allowing for partial restoration of wild-type response to osmotic stress. Our results show that the regulatory networks of bacteria can evolve new structures in ways that are both rapid and repeatable.
Highlights
Bacterial adaptation to environmental stress involves, in part, a modification of transcription patterns, with downstream impacts on physiological function
The hypothesis that the nature of the RpoS regulatory network creates an inherent conflict between stress protection and nutritional competence (SPANC) [3,4] provides a basis for predicting how natural selection acts on the global regulatory networks of E. coli
Despite the importance of this protein in response to some kinds of stresses, strains that lack a functional RpoS protein are found at appreciable frequency in nature
Summary
Bacterial adaptation to environmental stress involves, in part, a modification of transcription patterns, with downstream impacts on physiological function. Despite the importance of this protein in many environments, a functional RpoS seems to lower the ability of E. coli to scavenge for scarce nutrients [2,3] This cost is hypothesized to occur because there is a limiting amount of core RNA polymerase subunits in the cell, meaning that transcription of stress responsive, RpoS-dependent promoters will decrease the transcription from RpoS-independent promoters involved in nutrient acquisition and utilization [2,3,4]. The SPANC hypothesis predicts that natural selection will modify the network in favor of nutritional ability at the expense of stress resistance in some environments by decreasing or abolishing RpoS function. Strains with low- or null-activity rpoS alleles have been found in natural populations of E. coli and Salmonella enterica [3,7]
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