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...
| Main Authors: | , , , |
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| Format: | Journal article |
| Language: | English |
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Nature Publishing Group
2016
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| _version_ | 1797076601917145088 |
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| author | Sepil, I Carazo, P Perry, J Wigby, S |
| author_facet | Sepil, I Carazo, P Perry, J Wigby, S |
| author_sort | Sepil, I |
| collection | OXFORD |
| 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 melanogasterthat 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 wildtype 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. |
| first_indexed | 2024-03-07T00:06:01Z |
| format | Journal article |
| id | oxford-uuid:778fc98e-67f2-42a6-9caa-860768e0e4f9 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T00:06:01Z |
| publishDate | 2016 |
| publisher | Nature Publishing Group |
| record_format | dspace |
| spelling | oxford-uuid:778fc98e-67f2-42a6-9caa-860768e0e4f92022-03-26T20:24:57ZInsulin signalling mediates the response to male-induced harm in female Drosophila melanogaster.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:778fc98e-67f2-42a6-9caa-860768e0e4f9EnglishSymplectic Elements at OxfordNature Publishing Group2016Sepil, ICarazo, PPerry, JWigby, SGenetic 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 melanogasterthat 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 wildtype 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. |
| spellingShingle | Sepil, I Carazo, P Perry, J Wigby, S 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 |
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