title: Common mechanism underlies repeated evolution of extreme pollution tolerance.
abstract: Human alterations to the environment can exert strong evolutionary pressures, yet contemporary adaptation to human-mediated stressors is rarely documented in wildlife populations. A common-garden experimental design was coupled with comparative transcriptomics to discover evolved mechanisms enabling three populations of killifish resident in urban estuaries to survive normally lethal pollution exposure during development, and to test whether mechanisms are unique or common across populations. We show that killifish populations from these polluted sites have independently converged on a common adaptive mechanism, despite variation in contaminant profiles among sites. These populations are united by a similarly profound desensitization of aryl-hydrocarbon receptor-mediated transcriptional activation, which is associated with extreme tolerance to the lethal effects of toxic dioxin-like pollutants. The rapid, repeated, heritable and convergent nature of evolved tolerance suggests that ancestral killifish populations harboured genotypes that enabled adaptation to twentieth-century industrial pollutants.
authors: Department of Biological Sciences, Louisiana State University, 202 Life Sciences Building, Baton Rouge, LA 70803, USA. andreww@lsu.edu
authors: Andrew
authors: A
authors: Whitehead
authors: Whitney
authors: W
authors: Pilcher
authors: Denise
authors: D
authors: Champlin
authors: Diane
authors: D
authors: Nacci
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D018376:Cardiovascular Abnormalities / Q000139:chemically induced / Q000235:genetics / Q000473:pathology; D017753:Ecosystem; D019143:Evolution, Molecular; D023781:Fundulidae / Q000002:abnormalities / Q000235:genetics* / Q000378:metabolism; D020869:Gene Expression Profiling / Q000662:veterinary; D018507:Gene Expression Regulation, Developmental; D014644:Genetic Variation; D007928:Lethal Dose 50; D008873:Mid-Atlantic Region; D009511:New England; D010641:Phenotype; D011078:Polychlorinated Biphenyls / Q000633:toxicity*; D025341:Principal Component Analysis; D018336:Receptors, Aryl Hydrocarbon / Q000235:genetics / Q000378:metabolism; D014874:Water Pollutants, Chemical / Q000633:toxicity*
chemical_list: D018336:Receptors, Aryl Hydrocarbon; D014874:Water Pollutants, Chemical; D011078:Polychlorinated Biphenyls; C023035:3,4,5,3',4'-pentachlorobiphenyl