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Mitochondrial Dysfunction and Infection Generate Immunity–Fecundity Tradeoffs in Drosophila
Physiological responses to short-term environmental stressors, such as infection, can have long-term consequences for fitness, particularly if the responses are inappropriate or nutrient resources are limited. Genetic variation affecting energy acquisition, storage, and usage can limit cellular ener...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6145415/ https://www.ncbi.nlm.nih.gov/pubmed/29945242 http://dx.doi.org/10.1093/icb/icy078 |
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author | Buchanan, Justin L Meiklejohn, Colin D Montooth, Kristi L |
author_facet | Buchanan, Justin L Meiklejohn, Colin D Montooth, Kristi L |
author_sort | Buchanan, Justin L |
collection | PubMed |
description | Physiological responses to short-term environmental stressors, such as infection, can have long-term consequences for fitness, particularly if the responses are inappropriate or nutrient resources are limited. Genetic variation affecting energy acquisition, storage, and usage can limit cellular energy availability and may influence resource-allocation tradeoffs even when environmental nutrients are plentiful. Here, we utilized Drosophila mitochondrial–nuclear genotypes to test whether disrupted mitochondrial function interferes with nutrient-sensing pathways, and whether this disruption has consequences for tradeoffs between immunity and fecundity. We found that an energetically-compromised genotype was relatively resistant to rapamycin—a drug that targets nutrient-sensing pathways and mimics resource limitation. Dietary resource limitation decreased survival of energetically-compromised flies. Furthermore, survival of infection with a natural pathogen was decreased in this genotype, and females of this genotype experienced immunity–fecundity tradeoffs that were not evident in genotypic controls with normal energy metabolism. Together, these results suggest that this genotype may have little excess energetic capacity and fewer cellular nutrients, even when environmental nutrients are not limiting. Genetic variation in energy metabolism may therefore act to limit the resources available for allocation to life-history traits in ways that generate tradeoffs even when environmental resources are not limiting. |
format | Online Article Text |
id | pubmed-6145415 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-61454152018-09-25 Mitochondrial Dysfunction and Infection Generate Immunity–Fecundity Tradeoffs in Drosophila Buchanan, Justin L Meiklejohn, Colin D Montooth, Kristi L Integr Comp Biol Inside the Black Box: The Mitochondrial Basis of Life-history Variation and Animal Performance Physiological responses to short-term environmental stressors, such as infection, can have long-term consequences for fitness, particularly if the responses are inappropriate or nutrient resources are limited. Genetic variation affecting energy acquisition, storage, and usage can limit cellular energy availability and may influence resource-allocation tradeoffs even when environmental nutrients are plentiful. Here, we utilized Drosophila mitochondrial–nuclear genotypes to test whether disrupted mitochondrial function interferes with nutrient-sensing pathways, and whether this disruption has consequences for tradeoffs between immunity and fecundity. We found that an energetically-compromised genotype was relatively resistant to rapamycin—a drug that targets nutrient-sensing pathways and mimics resource limitation. Dietary resource limitation decreased survival of energetically-compromised flies. Furthermore, survival of infection with a natural pathogen was decreased in this genotype, and females of this genotype experienced immunity–fecundity tradeoffs that were not evident in genotypic controls with normal energy metabolism. Together, these results suggest that this genotype may have little excess energetic capacity and fewer cellular nutrients, even when environmental nutrients are not limiting. Genetic variation in energy metabolism may therefore act to limit the resources available for allocation to life-history traits in ways that generate tradeoffs even when environmental resources are not limiting. Oxford University Press 2018-09 2018-07-24 /pmc/articles/PMC6145415/ /pubmed/29945242 http://dx.doi.org/10.1093/icb/icy078 Text en © The Author(s) 2018. Published by Oxford University Press on behalf of the Society for Integrative and Comparative Biology. http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Inside the Black Box: The Mitochondrial Basis of Life-history Variation and Animal Performance Buchanan, Justin L Meiklejohn, Colin D Montooth, Kristi L Mitochondrial Dysfunction and Infection Generate Immunity–Fecundity Tradeoffs in Drosophila |
title | Mitochondrial Dysfunction and Infection Generate Immunity–Fecundity Tradeoffs in Drosophila |
title_full | Mitochondrial Dysfunction and Infection Generate Immunity–Fecundity Tradeoffs in Drosophila |
title_fullStr | Mitochondrial Dysfunction and Infection Generate Immunity–Fecundity Tradeoffs in Drosophila |
title_full_unstemmed | Mitochondrial Dysfunction and Infection Generate Immunity–Fecundity Tradeoffs in Drosophila |
title_short | Mitochondrial Dysfunction and Infection Generate Immunity–Fecundity Tradeoffs in Drosophila |
title_sort | mitochondrial dysfunction and infection generate immunity–fecundity tradeoffs in drosophila |
topic | Inside the Black Box: The Mitochondrial Basis of Life-history Variation and Animal Performance |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6145415/ https://www.ncbi.nlm.nih.gov/pubmed/29945242 http://dx.doi.org/10.1093/icb/icy078 |
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