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Sex‐dependent infection causes nonadditive effects on kissing bug fecundity
The influence of parasites on host reproduction has been widely studied in natural and experimental conditions. Most studies, however, have evaluated the parasite impact on female hosts only, neglecting the contribution of males for host reproduction. This omission is unfortunate as sex‐dependent in...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5433981/ https://www.ncbi.nlm.nih.gov/pubmed/28515890 http://dx.doi.org/10.1002/ece3.2956 |
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author | Botto‐Mahan, Carezza Campos, Verónica Medel, Rodrigo |
author_facet | Botto‐Mahan, Carezza Campos, Verónica Medel, Rodrigo |
author_sort | Botto‐Mahan, Carezza |
collection | PubMed |
description | The influence of parasites on host reproduction has been widely studied in natural and experimental conditions. Most studies, however, have evaluated the parasite impact on female hosts only, neglecting the contribution of males for host reproduction. This omission is unfortunate as sex‐dependent infection may have important implications for host–parasite associations. Here, we evaluate for the first time the independent and nonindependent effects of gender infection on host reproductive success using the kissing bug Mepraia spinolai and the protozoan Trypanosoma cruzi as model system. We set up four crossing treatments including the following: (1) both genders infected, (2) both genders uninfected, (3) males infected—females uninfected, and (4) males uninfected—females infected, using fecundity measures as response variables. Interactive effects of infection between sexes were prevalent. Uninfected females produced more and heavier eggs when crossed with uninfected than infected males. Uninfected males, in turn, sired more eggs and nymphs when crossed with uninfected than infected females. Unexpectedly, infected males sired more nymphs when crossed with infected than uninfected females. These results can be explained by the effect of parasitism on host body size. As infection reduced size in both genders, infection on one sex only creates body size mismatches and mating constraints that are not present in pairs with the same infection status. Our results indicate the fitness impact of parasitism was contingent on the infection status of genders and mediated by body size. As the fecundity impact of parasitism cannot be estimated independently for each gender, inferences based only on female host infection run the risk of providing biased estimates of parasite‐mediated impact on host reproduction. |
format | Online Article Text |
id | pubmed-5433981 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-54339812017-05-17 Sex‐dependent infection causes nonadditive effects on kissing bug fecundity Botto‐Mahan, Carezza Campos, Verónica Medel, Rodrigo Ecol Evol Original Research The influence of parasites on host reproduction has been widely studied in natural and experimental conditions. Most studies, however, have evaluated the parasite impact on female hosts only, neglecting the contribution of males for host reproduction. This omission is unfortunate as sex‐dependent infection may have important implications for host–parasite associations. Here, we evaluate for the first time the independent and nonindependent effects of gender infection on host reproductive success using the kissing bug Mepraia spinolai and the protozoan Trypanosoma cruzi as model system. We set up four crossing treatments including the following: (1) both genders infected, (2) both genders uninfected, (3) males infected—females uninfected, and (4) males uninfected—females infected, using fecundity measures as response variables. Interactive effects of infection between sexes were prevalent. Uninfected females produced more and heavier eggs when crossed with uninfected than infected males. Uninfected males, in turn, sired more eggs and nymphs when crossed with uninfected than infected females. Unexpectedly, infected males sired more nymphs when crossed with infected than uninfected females. These results can be explained by the effect of parasitism on host body size. As infection reduced size in both genders, infection on one sex only creates body size mismatches and mating constraints that are not present in pairs with the same infection status. Our results indicate the fitness impact of parasitism was contingent on the infection status of genders and mediated by body size. As the fecundity impact of parasitism cannot be estimated independently for each gender, inferences based only on female host infection run the risk of providing biased estimates of parasite‐mediated impact on host reproduction. John Wiley and Sons Inc. 2017-04-09 /pmc/articles/PMC5433981/ /pubmed/28515890 http://dx.doi.org/10.1002/ece3.2956 Text en © 2017 The Authors. Ecology and Evolution published by John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Botto‐Mahan, Carezza Campos, Verónica Medel, Rodrigo Sex‐dependent infection causes nonadditive effects on kissing bug fecundity |
title | Sex‐dependent infection causes nonadditive effects on kissing bug fecundity |
title_full | Sex‐dependent infection causes nonadditive effects on kissing bug fecundity |
title_fullStr | Sex‐dependent infection causes nonadditive effects on kissing bug fecundity |
title_full_unstemmed | Sex‐dependent infection causes nonadditive effects on kissing bug fecundity |
title_short | Sex‐dependent infection causes nonadditive effects on kissing bug fecundity |
title_sort | sex‐dependent infection causes nonadditive effects on kissing bug fecundity |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5433981/ https://www.ncbi.nlm.nih.gov/pubmed/28515890 http://dx.doi.org/10.1002/ece3.2956 |
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