Evolutionary and conservation biologists often use molecular markers to evaluate whether populations have experienced demographic bottlenecks that resulted in a loss of genetic variation. We evaluated the utility of microsatellites for detection of recent, severe bottlenecks and compared the amounts of genetic diversity lost in bottlenecks of different sizes. In experimental mesocosms, we established replicate populations by releasing 1, 2, 4 or 8 pairs of the western mosquitofish, Gambusia affinis (Poeciliidae). Using eight polymorphic microsatellite loci, we quantified seven indices of genetic diversity or change that have been used to assess the effects of demographic bottlenecks on populations. We compared indices for the experimentally bottlenecked populations to those for the source population and examined differences between populations established with different numbers of founders. Direct count heterozygosity and the proportion of polymorphic loci were not very sensitive to genetic changes that resulted from the experimental bottlenecks. Heterozygosity excess and expected heterozygosity were useful to varying degrees in the detection of bottlenecks. Allelic diversity and temporal variance in allele frequencies were most sensitive to genetic changes that resulted from the bottlenecks, and the temporal variance method was slightly more correlated with bottleneck size than was allelic diversity. Based on comparisons to a previous study with allozymes, heterozygosity, temporal variance in allele frequencies and allelic diversity, but not proportion of polymorphic loci, appear to be more sensitive to demographic bottlenecks when quantified using microsatellites. We found that analysis of eight highly polymorphic loci was sufficient to detect a recent demographic bottleneck and to obtain an estimate of the magnitude of bottleneck severity.
SummaryMolecular advances of the past decade have led to the discovery of a myriad of 'aging genes' ( methuselah , Indy , InR , Chico , superoxide dismutase ) that extend Drosophila lifespan by up to 85%. Despite this life extension, these mutants are no longer lived than at least some recently wildcaught strains. Typically, long-lived mutants are identified in relatively short-lived genetic backgrounds, and their effects are rarely tested in genetic backgrounds other than the one in which they were isolated or derived. However, the mutant's high-longevity phenotype may be dependent on interactions with alleles that are common in short-lived laboratory strains. Here we set out to determine whether one particular mutant could extend lifespan in long-lived genetic backgrounds in the fruit fly, Drosophila melanogaster . We measured longevity and resistance to thermal stress in flies that were transgenically altered to overexpress human superoxide dismutase ( SOD ) in the motorneurones in each of 10 genotypes. Each genotype carried the genetic background from a different naturally long-lived wild-caught Drosophila strain. While SOD increased lifespan on average, the effect was genotypeand sex-specific. Our results indicate that naturally segregating genes interact epistatically with the aging gene superoxide dismutase to modify its ability to extend longevity. This study points to the need to identify mutants that increase longevity not only in the lab strain of origin but also in naturally long-lived genetic backgrounds.
While there has been much recent focus on the ecological causes of adaptive diversification, we know less about the genetic nature of the trade-offs in resource use that create and maintain stable, diversified ecotypes. Here we show how a regulatory genetic change can contribute to sympatric diversification caused by differential resource use and maintained by negative frequency-dependent selection in Escherichia coli. During adaptation to sequential use of glucose and acetate, these bacteria differentiate into two ecotypes that differ in their growth profiles. The “slow-switcher” exhibits a long lag when switching to growth on acetate after depletion of glucose, whereas the “fast-switcher” exhibits a short switching lag. We show that the short switching time in the fast-switcher is associated with a failure to down-regulate potentially costly acetate metabolism during growth on glucose. While growing on glucose, the fast-switcher expresses malate synthase A (aceB), a critical gene for acetate metabolism that fails to be properly down-regulated because of a transposon insertion in one of its regulators. Swapping the mutant regulatory allele with the ancestral allele indicated that the transposon is in part responsible for the observed differentiation between ecological types. Our results provide a rare example of a mechanistic integration of diversifying processes at the genetic, physiological, and ecological levels.
Understanding the mechanisms and processes that generate biological diversity is a fundamental problem in evolution and ecology. In the past decade, the theory of evolutionary branching and adaptive diversification has provided new perspectives for understanding the evolution of diversity caused by ecological interactions. In models of adaptive diversification, the fitness landscapes change dynamically, so that the likelihood of diversification into different phenotypic clusters increases over time. In contrast, in models with static fitness landscapes, the likelihood of diversification decreases as populations climb fitness peaks, because crossing maladaptive fitness valleys becomes increasingly difficult. We used experimental evolution in bacteria to test how the likelihood of diversification changes over time in a bacterial lineage that has diversified in sympatry from a single ancestral strain. By analyzing the ''fossil'' record of this lineage, and restarting the lineage from different time points in the evolutionary past, we demonstrate that: (i) the lineage has initially undergone a phase of directional adaptation to the competitive environment, and (ii) during this phase, the likelihood of diversification increases significantly over time. These results suggest evolutionary branching caused by frequency-dependent competition as the main mechanism of diversification in our experimental populations.Escherichia coli ͉ evolutionary branching ͉ experimental evolution ͉ frequency dependence D iversification is thought to occur when descendent populations come to occupy different ecological niches. This situation is formalized by adaptive landscapes, in which different peaks correspond to different niches (1-5). When fitness landscapes are static and fixed over time, diversification can occur when an ancestral population is near a trough in such a landscape, and different subpopulations evolve toward different fitness peaks. In this case, it becomes increasingly difficult to cross the fitness valleys if the ancestral population evolves up a fitness peak. As a consequence, diversification becomes less likely with increasing adaptation (1, 6-8).In contrast, if the fitness landscape depends on the current position of the population in phenotype space, i.e., if selection is frequency-dependent, the landscape changes as the population evolves. In this case, new niches (i.e., fitness peaks) may only open up as the population progresses along its evolutionary trajectory, and hence diversification may become more likely over time. An elegant framework for describing diversification when selection is frequency-dependent is provided by the theory of adaptive dynamics (9-11), in which adaptive diversification is described by the mathematical phenomenon of evolutionary branching (10). When a population undergoes evolutionary branching, it first converges under directional selection toward a point in phenotype space at which selection turns disruptive because of frequency-dependent interactions. From this evolutionary branc...
BackgroundThe evolutionary consequences of competition are of great interest to researchers studying sympatric speciation, adaptive radiation, species coexistence and ecological assembly. Competition's role in driving evolutionary change in phenotypic distributions, and thus causing ecological character displacement, has been inferred from biogeographical data and measurements of divergent selection on a focal species in the presence of competitors. However, direct experimental demonstrations of character displacement due to competition are rare.ResultsWe demonstrate a causal role for competition in ecological character displacement. Using populations of the bacterium Escherichia coli that have adaptively diversified into ecotypes exploiting different carbon resources, we show that when interspecific competition is relaxed, phenotypic distributions converge. When we reinstate competition, phenotypic distributions diverge.ConclusionThis accordion-like dynamic provides direct experimental evidence that competition for resources can cause evolutionary shifts in resource-related characters.
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