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Theory predicts that organisms should diversify their offspring when faced with a stressful environment. This prediction has received empirical support across diverse groups of organisms and stressors. For example, when encountered byCaenorhabditis elegansduring early development, food limitation (a common environmental stressor) induces the nematodes to arrest in a developmental stage called dauer and to increase their propensity to outcross when they are subsequently provided with food and enabled to develop to maturity. Here we tested whether food limitation first encountered during late development/early adulthood can also induce increased outcrossing propensity inC. elegans. Previously well‐fedC. elegansincreased their propensity to outcross when challenged with food limitation during the final larval stage of development and into early adulthood, relative to continuously well‐fed (control) nematodes. Our results thus support previous research demonstrating that the stress of food limitation can induce increased outcrossing propensity inC. elegans. Furthermore, our results expand on previous work by showing that food limitation can still increase outcrossing propensity even when it is not encountered until late development, and this can occur independently of the developmental and gene expression changes associated with dauer.

 

Biparental sex is widespread in nature, yet costly relative to uniparental reproduction. It is generally unclear why self-fertilizing or asexual lineages do not readily invade outcrossing populations. The Red Queen hypothesis predicts that coevolving parasites can prevent self-fertilizing or asexual lineages from invading outcrossing host populations. However, only highly virulent parasites are predicted to maintain outcrossing, which may limit the general applicability of the Red Queen hypothesis. Here, we tested whether the ability of coevolving parasites to prevent invasion of self-fertilization within outcrossing host populations was dependent on parasite virulence. We introduced wild-type Caenorhabditis elegans hermaphrodites, capable of both self-fertilization and outcrossing, into C. elegans populations fixed for a mutant allele conferring obligate outcrossing. Replicate C. elegans populations were exposed for 24 host generations to one of four strains of Serratia marcescens parasites that varied in virulence, under three treatments: a heat-killed (control, noninfectious) parasite treatment, a fixed-genotype (nonevolving) parasite treatment, and a copassaged (potentially coevolving) parasite treatment. As predicted, self-fertilization invaded C. elegans host populations in the control and fixed-parasite treatments, regardless of parasite virulence. In the copassaged treatment, selfing invaded host populations coevolving with low- to mid-virulence strains, but remained rare in hosts coevolving with highly virulent bacterial strains. Therefore, we found that only highly virulent coevolving parasites can impede the invasion of selfing.

 

Gene flow into populations can increase additive genetic variation and introduce novel beneficial alleles, thus facilitating adaptation. However, gene flow may also impede adaptation by disrupting beneficial genotypes, introducing deleterious alleles, or creating novel dominant negative interactions. While theory and fieldwork have provided insight into the effects of gene flow, direct experimental tests are rare. Here, we evaluated the effects of gene flow on adaptation in the nematode Caenorhabditis elegans during exposure to the bacterial parasite, Serratia marcescens. We evolved hosts against nonevolving parasites for 10 passages while controlling host gene flow and source population. We used source nematode populations with three different genetic backgrounds (one similar to the sink population and two different) and two evolutionary histories (previously adapted to S. marcescens or naive). We found that populations with gene flow exhibited greater increases in parasite resistance than those without gene flow. Additionally, gene flow from adapted populations resulted in greater increases in resistance than gene flow from naive populations, particularly with gene flow from novel genetic backgrounds. Overall, this work demonstrates that gene flow can facilitate adaptation and suggests that the genetic architecture and evolutionary history of source populations can alter the sink population’s response to selection.

 

Many interspecific interactions are shaped by coevolution. Transmission mode is thought to influence opportunities for coevolution within symbiotic interactions. Vertical transmission maintains partner fidelity, increasing opportunities for coevolution, but horizontal transmission may disrupt partner fidelity, potentially reducing opportunities for coevolution. Despite these predictions, the role of coevolution in the maintenance of horizontally transmitted symbioses is unclear. Leveraging a tractable insect–bacteria symbiosis, we tested for signatures of pairwise coevolution by assessing patterns of host–symbiont specialization. If pairwise coevolution defines the interaction, we expected to observe evidence of reciprocal specialization between hosts and their local symbionts. We found no evidence for local adaptation between sympatric lineages of Anasa tristis squash bugs and Caballeronia spp. symbionts across their native geographic range. We also found no evidence for specialization between three co-localized Anasa host species and their native Caballeronia symbionts. Our results demonstrate generalist dynamics underlie the interaction between Anasa insect hosts and their Caballeronia symbionts. We predict that selection from multiple host species may favor generalist symbiont traits through diffuse coevolution. Alternatively, selection for generalist traits may be a consequence of selection by hosts for fixed cooperative symbiont traits without coevolution.

 

Host populations often evolve defenses against parasites due to the significant fitness costs imposed by infection. However, adaptation to a specific parasite may alter the effectiveness of the host’s defenses in general. Consequently, the specificity of host defense may be influenced by a host population’s evolutionary history with parasites. Further, the degree of reciprocal change within an interaction may profoundly alter the range of host defense, given that antagonistic coevolutionary interactions are predicted to favor defense against specific parasite genotypes. Here, we examined the effect of host evolutionary history on host defense range by assessing the mortality rates of Caenorhabditis elegans host populations exposed to an array of Serratia marcescens bacterial parasite strains. Importantly, each of the host populations were derived from the same genetic background but have different experimental evolution histories with parasites. Each of these histories (exposure to either heat-killed, fixed genotype, or coevolving parasites) carries a different level of evolutionary reciprocity. Overall, we observed an effect of host evolutionary history in that previously coevolved host populations were generally the most susceptible to novel parasite strains. This data demonstrates that host evolutionary history can have a significant impact on host defense, and that host-parasite coevolution can increase host susceptibility to novel parasites. 

In the past three decades, laboratory natural selection has become a widely used technique in biological research. Most studies which have utilized this technique are in the realm of basic science, often testing hypotheses related to mechanisms of evolutionary change or ecological dynamics. While laboratory natural selection is currently utilized heavily in this setting, there is a significant gap with its usage in applied studies, especially when compared to the other selection experiment methodologies like artificial selection and directed evolution. This is despite avenues of research in the applied sciences which seem well suited to laboratory natural selection. In this review, we place laboratory natural selection in context with other selection experiments, identify the characteristics which make it well suited for particular kinds of applied research and briefly cover key examples of the usefulness of selection experiments within applied science. Finally, we identify three promising areas of inquiry for laboratory natural selection in the applied sciences: bioremediation technology, identifying mechanisms of drug resistance and optimizing biofuel production. Although laboratory natural selection is currently less utilized in applied science when compared to basic research, the method has immense promise in the field moving forward.

 

A core hypothesis in coevolutionary theory proposes that parasites adapt to specifically infect common host genotypes. Under this hypothesis, parasites function as agents of negative frequency-dependent selection, favouring rare host genotypes. This parasite-mediated advantage of rarity is key to the idea that parasites maintain genetic variation and select for outcrossing in host populations. Here, we report the results of an experimental test of parasite adaptation to common versus rare host genotypes. We selected the bacterial parasite Serratia marcescens to kill Caenorhabdiis elegans hosts in uneven mixtures of host genotypes. To examine the effect of commonness itself, independent of host identity, each of four host genotypes was represented as common or rare in experimental host mixtures. After experimental selection, we evaluated a parasite line's change in virulence—the selected fitness trait—on its rare and common host genotypes. Our results were consistent with a slight advantage for rare host genotypes: on average, parasites lost virulence against rare genotypes but not against common genotypes. The response varied substantially, however, with distinct patterns across host genotype mixtures. These findings support the potential for parasites to impose negative frequency-dependent selection, while emphasizing that the cost of being common may vary with host genotype. 

Despite the ubiquity and importance of mutualistic interactions, we know little about the evolutionary genetics underlying their long‐term persistence. As in antagonistic interactions, mutualistic symbioses are characterized by substantial levels of phenotypic and genetic diversity. In contrast to antagonistic interactions, however, we, by and large, do not understand how this variation arises, how it is maintained, nor its implications for future evolutionary change. Currently, we rely on phenotypic models to address the persistence of mutualistic symbioses, but the success of an interaction almost certainly depends heavily on genetic interactions. In this review, we argue that evolutionary genetic models could provide a framework for understanding the causes and consequences of diversity and why selection may favour processes that maintain variation in mutualistic interactions.