Insulin signalling mediates the response to male-induced harm in female Drosophila melanogaster

Sepil, Irem, Carazo, Pau, Perry, Jennifer C. ORCID: https://orcid.org/0000-0002-8449-2764 and Wigby, Stuart (2016) Insulin signalling mediates the response to male-induced harm in female Drosophila melanogaster. Scientific Reports, 6. ISSN 2045-2322

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Abstract

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.

Item Type: Article
Additional Information: Funding Information: We would like to thank Sarah Knowles and Tobias Uller for helpful advice. I.S. and S.W. were supported by a BBSRC fellowship to S.W. (BB/K014544/1). P.C. was supported by an FP7 IEF Marie Curie fellowship (PIEF-GA-2010-273010) from the European Commission. J.C.P. was supported by a fellowship from Jesus College (University of Oxford).
Uncontrolled Keywords: general ,/dk/atira/pure/subjectarea/asjc/1000
Faculty \ School: Faculty of Science > School of Biological Sciences
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Depositing User: LivePure Connector
Date Deposited: 01 Nov 2022 16:31
Last Modified: 01 Nov 2022 16:31
URI: https://ueaeprints.uea.ac.uk/id/eprint/89494
DOI: 10.1038/srep30205

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