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Common Mechanism Underlies Repeated Evolution of Extreme Pollution Tolerance
Citation:
WHITEHEAD, A., W. PILCHER, D. M. CHAMPLIN, AND D. E. NACCI. Common Mechanism Underlies Repeated Evolution of Extreme Pollution Tolerance. Proceedings of the Royal Society B. Royal Society Publishing, London, Uk, 279(1728):427-433, (2012).
Impact/Purpose:
This manuscript describes experimental studies that contribute to our understanding of the ecological risks associated with chronic contaminant exposures to wildlife populations. Here, we assessed genome wide expression patterns, or transcriptomics, in response to an important class of environmental pollutants to which tolerance has evolved in an estuarine fish species resident to estuaries of the Atlantic U.S. coast. We used laboratory studies to characterize variation in gene expression among laboratory-reared progeny of fish from populations known to vary in their sensitivity to certain pollutants to infer mechanisms of toxicity and tolerance. Results of these studies demonstrate the value of comparative transcriptomics to diagnose and predict effects of chemical stressors and characterize the mechanisms and costs of toxic and compensatory responses to chemical stressors by wild populations. General impacts from this contribution include improved understanding by managers and scientists of links between human activities, natural dynamics, ecological stressors and ecosystem condition.
Description:
Human alterations to the environment can exert strong evolutionary pressures, yet contemporary adaptation to human-mediated stressors is rarely documented in wild 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 pollution exposure during development, and to test whether mechanisms are unique or common across populations. We show that populations from polluted sites have independently converged on a common adaptive mechanism, despite variation in contaminant profiles among sites. These populations are united by similarly profound desensitization of aryl-hydrocarbon receptor (AHR) 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 harbored genotypes that enabled adaptation to 20th century industrial pollutants.