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The genetic architecture of phenotypic traits can affect the mode and tempo of trait evolution. Human‐altered environments can impose strong natural selection, where successful evolutionary adaptation requires swift and large phenotypic shifts. In these scenarios, theory predicts that adaptation is due to a few adaptive variants of large effect, but empirical studies that have revealed the genetic architecture of rapidly evolved phenotypes are rare, especially for populations inhabiting polluted environments.Funduluskillifish have repeatedly evolved adaptive resistance to extreme pollution in urban estuaries. Prior studies, including genome scans for signatures of natural selection, have revealed some of the genes and pathways important for evolved pollution resistance, and provide context for the genotype–phenotype association studies reported here. We created multiple quantitative trait locus (QTL) mapping families using progenitors from four different resistant populations, and using RAD‐seq genetically mapped variation in sensitivity (developmental perturbations) following embryonic exposure to a model toxicant PCB‐126. We found that one to two large‐effect QTL loci accounted for resistance to PCB‐mediated developmental toxicity. QTLs harbored candidate genes that govern the regulation of aryl hydrocarbon receptor (AHR) signaling. One QTL locus was shared across all populations and another was shared across three populations. One QTL locus showed strong signatures of recent natural selection in the corresponding wild population but another QTL locus did not. Some candidate genes for PCB resistance inferred from genome scans in wild populations were identified as QTL, but some key candidate genes were not. We conclude that rapidly evolved resistance to the developmental defects normally caused by PCB‐126 is governed by few genes of large effect. However, other aspects of resistance beyond developmental phenotypes may be governed by additional loci, such that comprehensive resistance to PCB‐126, and to the mixtures of chemicals that distinguish urban estuaries more broadly, may be more genetically complex.

 

Populations of the non-migratory estuarine fish Fundulus heteroclitus inhabiting the heavily polluted New Bedford Harbour (NBH) estuary have shown inherited tolerance to local pollutants introduced to their habitats in the past 100 years. Here we examine two questions: (i) Is there pollution-driven selection on the mitochondrial genome across a fine geographical scale? and (ii) What is the pattern of migration among sites spanning a strong pollution gradient? Whole mitochondrial genomes were analysed for 133 F. heteroclitus from seven nearby collection sites: four sites along the NBH pollution cline (approx. 5 km distance), which had pollution-adapted fish, as well as one site adjacent to the pollution cline and two relatively unpolluted sites about 30 km away, which had pollution-sensitive fish. Additionally, we used microsatellite analyses to quantify genetic variation over three F. heteroclitus generations in both pollution-adapted and sensitive individuals collected from two sites at two different time points (1999/2000 and 2007/2008). Our results show no evidence for a selective sweep of mtDNA in the polluted sites. Moreover, mtDNA analyses revealed that both pollution-adapted and sensitive populations harbour similar levels of genetic diversity. We observed a high level of non-synonymous mutations in the most polluted site. This is probably associated with a reduction in N e and concomitant weakening of purifying selection, a demographic expansion following a pollution-related bottleneck or increased mutation rates. Our demographic analyses suggest that isolation by distance influences the distribution of mtDNA genetic variation between the pollution cline and the clean populations at broad spatial scales. At finer scales, population structure is patchy, and neither spatial distance, pollution concentration or pollution tolerance is a good predictor of mtDNA variation. Lastly, microsatellite analyses revealed stable population structure over the last decade. 

Linking organismal‐level processes to underlying suborganismal mechanisms at the molecular, cellular and organ level constitutes a major challenge for predictive ecological risk assessments. This challenge can be addressed with the simple bioenergetic models in the family of dynamic energy budget (DEB), which consist of a small number of state equations quantifying universal processes, such as feeding, maintenance, development, reproduction and growth.

Motivated by the need for process‐based models to evaluate the impact of endocrine disruptors on ecologically relevant endpoints, this paper develops and evaluates two general modelling modules describing demand‐driven feedback mechanisms within the DEB modelling framework exerted by gonads on the allocation of resources to production of reproductive matter.

These modules describe iteroparous, semelparous and batch‐mode reproductive strategies. The modules have a generic form with both positive and negative feedback components; species‐ and sex‐specific attributes of endocrine regulation can be added without changing the core of the modules.

We demonstrate that these modules successfully describe time‐resolved measurements of wet weight of body, ovaries and liver, egg diameter and plasma content of vitellogenin and oestradiol in rainbow trout (Oncorynchus mykiss) by fitting these models to published and new data, which require the estimation of less than two parameters per data type.

We illustrate the general applicability of the concept of demand‐driven allocation of resources to reproduction by evaluating one of the modules with data on growth and seed production of an annual plant, the common bean (Phaseolisvulgaris).

Aplain language summaryis available for this article.

 

Atlantic killifish (Fundulus heteroclitus) residing in some urban and industrialized estuaries of theUSeastern seaboard demonstrate recently evolved and extreme tolerance to toxic aryl hydrocarbon pollutants, characterized as dioxin‐like compounds (DLCs). Here, we provide an unusually comprehensive accounting (69%) through quantitative trait locus (QTL) analysis of the genetic basis forDLCtolerance in killifish inhabiting an urban estuary contaminated withPCBcongeners, the most toxic of which areDLCs. Consistent with mechanistic knowledge ofDLCtoxicity in fish and other vertebrates, the aryl hydrocarbon receptor (ahr2) region accounts for 17% of trait variation; however,QTLon independent linkage groups and their interactions have even greater explanatory power (44%).QTLinterpreted within the context of recently availableFundulusgenomic resources and shared synteny among fish species suggest adaptation via interacting components of a complex stress response network. SomeQTLwere also enriched in other killifish populations characterized asDLC‐tolerant and residing in distant urban estuaries contaminated with unique mixtures of pollutants. Together, our results suggest thatDLCtolerance in killifish represents an emerging example of parallel contemporary evolution that has been driven by intense human‐mediated selection on natural populations.