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Convergent evolution of toxin resistance in animals

Convergence is the phenomenon whereby similar phenotypes evolve independently in different lineages. One example is resistance to toxins in animals. Toxins have evolved many times throughout the tree of life. They disrupt molecular and physiological pathways in target species, thereby incapacitating...

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Autores principales: van Thiel, Jory, Khan, Muzaffar A., Wouters, Roel M., Harris, Richard J., Casewell, Nicholas R., Fry, Bryan G., Kini, R. Manjunatha, Mackessy, Stephen P., Vonk, Freek J., Wüster, Wolfgang, Richardson, Michael K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9543476/
https://www.ncbi.nlm.nih.gov/pubmed/35580905
http://dx.doi.org/10.1111/brv.12865
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author van Thiel, Jory
Khan, Muzaffar A.
Wouters, Roel M.
Harris, Richard J.
Casewell, Nicholas R.
Fry, Bryan G.
Kini, R. Manjunatha
Mackessy, Stephen P.
Vonk, Freek J.
Wüster, Wolfgang
Richardson, Michael K.
author_facet van Thiel, Jory
Khan, Muzaffar A.
Wouters, Roel M.
Harris, Richard J.
Casewell, Nicholas R.
Fry, Bryan G.
Kini, R. Manjunatha
Mackessy, Stephen P.
Vonk, Freek J.
Wüster, Wolfgang
Richardson, Michael K.
author_sort van Thiel, Jory
collection PubMed
description Convergence is the phenomenon whereby similar phenotypes evolve independently in different lineages. One example is resistance to toxins in animals. Toxins have evolved many times throughout the tree of life. They disrupt molecular and physiological pathways in target species, thereby incapacitating prey or deterring a predator. In response, molecular resistance has evolved in many species exposed to toxins to counteract their harmful effects. Here, we review current knowledge on the convergence of toxin resistance using examples from a wide range of toxin families. We explore the evolutionary processes and molecular adaptations driving toxin resistance. However, resistance adaptations may carry a fitness cost if they disrupt the normal physiology of the resistant animal. Therefore, there is a trade‐off between maintaining a functional molecular target and reducing toxin susceptibility. There are relatively few solutions that satisfy this trade‐off. As a result, we see a small set of molecular adaptations appearing repeatedly in diverse animal lineages, a phenomenon that is consistent with models of deterministic evolution. Convergence may also explain what has been called ‘autoresistance’. This is often thought to have evolved for self‐protection, but we argue instead that it may be a consequence of poisonous animals feeding on toxic prey. Toxin resistance provides a unique and compelling model system for studying the interplay between trophic interactions, selection pressures and the molecular mechanisms underlying evolutionary novelties.
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spelling pubmed-95434762022-10-14 Convergent evolution of toxin resistance in animals van Thiel, Jory Khan, Muzaffar A. Wouters, Roel M. Harris, Richard J. Casewell, Nicholas R. Fry, Bryan G. Kini, R. Manjunatha Mackessy, Stephen P. Vonk, Freek J. Wüster, Wolfgang Richardson, Michael K. Biol Rev Camb Philos Soc Original Articles Convergence is the phenomenon whereby similar phenotypes evolve independently in different lineages. One example is resistance to toxins in animals. Toxins have evolved many times throughout the tree of life. They disrupt molecular and physiological pathways in target species, thereby incapacitating prey or deterring a predator. In response, molecular resistance has evolved in many species exposed to toxins to counteract their harmful effects. Here, we review current knowledge on the convergence of toxin resistance using examples from a wide range of toxin families. We explore the evolutionary processes and molecular adaptations driving toxin resistance. However, resistance adaptations may carry a fitness cost if they disrupt the normal physiology of the resistant animal. Therefore, there is a trade‐off between maintaining a functional molecular target and reducing toxin susceptibility. There are relatively few solutions that satisfy this trade‐off. As a result, we see a small set of molecular adaptations appearing repeatedly in diverse animal lineages, a phenomenon that is consistent with models of deterministic evolution. Convergence may also explain what has been called ‘autoresistance’. This is often thought to have evolved for self‐protection, but we argue instead that it may be a consequence of poisonous animals feeding on toxic prey. Toxin resistance provides a unique and compelling model system for studying the interplay between trophic interactions, selection pressures and the molecular mechanisms underlying evolutionary novelties. Blackwell Publishing Ltd 2022-05-17 2022-10 /pmc/articles/PMC9543476/ /pubmed/35580905 http://dx.doi.org/10.1111/brv.12865 Text en © 2022 The Authors. Biological Reviews published by John Wiley & Sons Ltd on behalf of Cambridge Philosophical Society. https://creativecommons.org/licenses/by-nc/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Original Articles
van Thiel, Jory
Khan, Muzaffar A.
Wouters, Roel M.
Harris, Richard J.
Casewell, Nicholas R.
Fry, Bryan G.
Kini, R. Manjunatha
Mackessy, Stephen P.
Vonk, Freek J.
Wüster, Wolfgang
Richardson, Michael K.
Convergent evolution of toxin resistance in animals
title Convergent evolution of toxin resistance in animals
title_full Convergent evolution of toxin resistance in animals
title_fullStr Convergent evolution of toxin resistance in animals
title_full_unstemmed Convergent evolution of toxin resistance in animals
title_short Convergent evolution of toxin resistance in animals
title_sort convergent evolution of toxin resistance in animals
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9543476/
https://www.ncbi.nlm.nih.gov/pubmed/35580905
http://dx.doi.org/10.1111/brv.12865
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