Cargando…

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...

Descripción completa

Detalles Bibliográficos
Autores principales: Buchanan, Justin L, Meiklejohn, Colin D, Montooth, Kristi L
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2018
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
_version_ 1783356261976244224
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
work_keys_str_mv AT buchananjustinl mitochondrialdysfunctionandinfectiongenerateimmunityfecunditytradeoffsindrosophila
AT meiklejohncolind mitochondrialdysfunctionandinfectiongenerateimmunityfecunditytradeoffsindrosophila
AT montoothkristil mitochondrialdysfunctionandinfectiongenerateimmunityfecunditytradeoffsindrosophila