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Insulin signalling mediates the response to male-induced harm in female Drosophila melanogaster
Genetic manipulations in nutrient-sensing pathways are known to both extend lifespan and modify responses to environmental stressors (e.g., starvation, oxidative and thermal stresses), suggesting that similar mechanisms regulate lifespan and stress resistance. However, despite being a key factor red...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4960482/ https://www.ncbi.nlm.nih.gov/pubmed/27457757 http://dx.doi.org/10.1038/srep30205 |
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author | Sepil, Irem Carazo, Pau Perry, Jennifer C. Wigby, Stuart |
author_facet | Sepil, Irem Carazo, Pau Perry, Jennifer C. Wigby, Stuart |
author_sort | Sepil, Irem |
collection | PubMed |
description | Genetic manipulations in nutrient-sensing pathways are known to both extend lifespan and modify responses to environmental stressors (e.g., starvation, oxidative and thermal stresses), suggesting that similar mechanisms regulate lifespan and stress resistance. However, despite being a key factor reducing female lifespan and affecting female fitness, male-induced harm has rarely been considered as a stressor mediated by nutrient sensing pathways. We explored whether a lifespan-extending manipulation also modifies female resistance to male-induced harm. To do so, we used long-lived female Drosophila melanogaster that had their insulin signalling pathway downregulated by genetically ablating the median neurosecretory cells (mNSC). We varied the level of exposure to males for control and ablated females and tested for interacting effects on female lifespan and fitness. As expected, we found that lifespan significantly declined with exposure to males. However, mNSC-ablated females maintained significantly increased lifespan across all male exposure treatments. Furthermore, lifespan extension and relative fitness of mNSC-ablated females were maximized under intermediate exposure to males, and minimized under low and high exposure to males. Overall, our results suggest that wild-type levels of insulin signalling reduce female susceptibility to male-induced harm under intense sexual conflict, and may also protect females when mating opportunities are sub-optimally low. |
format | Online Article Text |
id | pubmed-4960482 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-49604822016-08-04 Insulin signalling mediates the response to male-induced harm in female Drosophila melanogaster Sepil, Irem Carazo, Pau Perry, Jennifer C. Wigby, Stuart Sci Rep Article Genetic manipulations in nutrient-sensing pathways are known to both extend lifespan and modify responses to environmental stressors (e.g., starvation, oxidative and thermal stresses), suggesting that similar mechanisms regulate lifespan and stress resistance. However, despite being a key factor reducing female lifespan and affecting female fitness, male-induced harm has rarely been considered as a stressor mediated by nutrient sensing pathways. We explored whether a lifespan-extending manipulation also modifies female resistance to male-induced harm. To do so, we used long-lived female Drosophila melanogaster that had their insulin signalling pathway downregulated by genetically ablating the median neurosecretory cells (mNSC). We varied the level of exposure to males for control and ablated females and tested for interacting effects on female lifespan and fitness. As expected, we found that lifespan significantly declined with exposure to males. However, mNSC-ablated females maintained significantly increased lifespan across all male exposure treatments. Furthermore, lifespan extension and relative fitness of mNSC-ablated females were maximized under intermediate exposure to males, and minimized under low and high exposure to males. Overall, our results suggest that wild-type levels of insulin signalling reduce female susceptibility to male-induced harm under intense sexual conflict, and may also protect females when mating opportunities are sub-optimally low. Nature Publishing Group 2016-07-26 /pmc/articles/PMC4960482/ /pubmed/27457757 http://dx.doi.org/10.1038/srep30205 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Sepil, Irem Carazo, Pau Perry, Jennifer C. Wigby, Stuart Insulin signalling mediates the response to male-induced harm in female Drosophila melanogaster |
title | Insulin signalling mediates the response to male-induced harm in female Drosophila melanogaster |
title_full | Insulin signalling mediates the response to male-induced harm in female Drosophila melanogaster |
title_fullStr | Insulin signalling mediates the response to male-induced harm in female Drosophila melanogaster |
title_full_unstemmed | Insulin signalling mediates the response to male-induced harm in female Drosophila melanogaster |
title_short | Insulin signalling mediates the response to male-induced harm in female Drosophila melanogaster |
title_sort | insulin signalling mediates the response to male-induced harm in female drosophila melanogaster |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4960482/ https://www.ncbi.nlm.nih.gov/pubmed/27457757 http://dx.doi.org/10.1038/srep30205 |
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