Environmental heterogeneity may be a general explanation for both the quantity of genetic variation in populations and the ecological niche width of individuals. To evaluate this hypothesis, I review the literature on selection experiments in heterogeneous environments. The niche width usually – but not invariably – evolves to match the amount of environmental variation, specialists evolving in homogeneous environments and generalists evolving in heterogeneous environments. The genetics of niche width are more complex than has previously been recognized, particularly with respect to the magnitude of costs of adaptation and the putative constraints on the evolution of generalists. Genetic variation in fitness is more readily maintained in heterogeneous environments than in homogeneous environments and this diversity is often stably maintained through negative frequency‐dependent selection. Moreover environmental heterogeneity appears to be a plausible mechanism for at least two well‐known patterns of species diversity at the landscape scale. I conclude that environmental heterogeneity is a plausible and possibly very general explanation for diversity across the range of scales from individuals to landscapes.

Antibiotic resistance is increasing in pathogenic microbial populations and is thus a major threat to public health. The fate of a resistance mutation in pathogen populations is determined in part by its fitness. Mutations that suffer little or no fitness cost are more likely to persist in the absence of antibiotic treatment. In this review, we performed a meta-analysis to investigate the fitness costs associated with single mutational events that confer resistance. Generally, these mutations were costly, although several drug classes and species of bacteria on average did not show a cost. Further investigations into the rate and fitness values of compensatory mutations that alleviate the costs of resistance will help us to better understand both the emergence and management of antibiotic resistance in clinical settings.

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The extent to which a population diverges from its ancestor through adaptive evolution depends on variation supplied by novel beneficial mutations. Extending earlier work, recent theory makes two predictions that seem to be robust to biological details: the distribution of fitness effects among beneficial mutations before selection should be (i) exponential and (ii) invariant, meaning it is always exponential regardless of the fitness rank of the wild-type allele. Here we test these predictions by assaying the fitness of 665 independently derived single-step mutations in the bacterium Pseudomonas fluorescens across a range of environments. We show that the distribution of fitness effects among beneficial mutations is indistinguishable from an exponential despite marked variation in the fitness rank of the wild type across environments. These results suggest that the initial step in adaptive evolution--the production of novel beneficial mutants from which selection sorts--is very general, being characterized by an approximately exponential distribution with many mutations of small effect and few of large effect. We also document substantial variation in the pleiotropic costs of antibiotic resistance, a result that may have implications for strategies aimed at eliminating resistant pathogens in animal and human populations.

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.

Much of life's diversity is thought to have arisen through successive rounds of adaptive radiation-the rapid diversification of a lineage into a range of ecologically and phenotypically distinct species. Both resource competition and predation have been suggested as mechanisms driving this process, although the former is better studied than the latter. Here we show experimentally how predation by a protist, Tetrahymena thermophila, affects diversification in a model adaptive radiation of the bacterial prey, Pseudomonas fluorescens. We estimate the frequency-dependent fitness functions of competing niche-specialist prey in the presence and absence of predation, and use these to test hypotheses about the extent (measured as the number of new genotypes) and rate of diversification. Competition and predation independently generated diversifying selection that we show is capable of driving prey diversification to similar extents but at different rates, diversification being markedly delayed in the presence of predators. The cause of this delay stems from weaker diversifying selection due to the reduction in prey density caused by predation. Our results suggest that predation may play an under-appreciated role in driving adaptive radiations.

The species diversity of natural communities is often strongly related to their productivity. The pattern of this relationship seems to vary: diversity is known to increase monotonically with productivity, to decrease monotonically with productivity, and to be unimodally related to productivity, with maximum diversity occurring at intermediate levels of productivity. The mechanism underlying these patterns remains obscure, although many possibilities have been suggested. Here we outline a simple mechanism--involving selection in a heterogeneous environment--to explain these patterns, and test it using laboratory cultures of the bacterium Pseudomonas fluorescens. We grew diverse cultures over a wide range of nutrient concentrations, and found a strongly unimodal relationship between diversity and productivity in heterogeneous, but not in homogeneous, environments. Our result provides experimental evidence that the unimodal relationship often observed in natural communities can be caused by selection for specialized types in a heterogeneous environment.

External agents of mortality (disturbances) occur over a wide range of scales of space and time, and are believed to have large effects on species diversity. The "intermediate disturbance hypothesis", which proposes maximum diversity at intermediate frequencies of disturbance, has received support from both field and laboratory studies. Coexistence of species at intermediate frequencies of disturbance is thought to require trade-offs between competitive ability and disturbance tolerance, and a metapopulation structure, with disturbance affecting only a few patches at any given time. However, a unimodal relationship can also be generated by global disturbances that affect all patches simultaneously, provided that the environment contains spatial niches to which different species are adapted. Here we report the results of tests of this model using both isogenic and diverse populations of the bacterium Pseudomonas fluorescens. In both cases, a unimodal relationship between diversity and disturbance frequency was generated in heterogeneous, but not in homogeneous, environments. The cause of this relationship is competition among niche-specialist genotypes, which maintains diversity at intermediate disturbance, but not at high or low disturbance. Our results show that disturbance can modulate the effect of spatial heterogeneity on biological diversity in natural environments.