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Data from: Experimental evolution demonstrates evolvability of preferential nutrient allocation to competing traits, in response to chronic malnutrition.

Citation

Vijendravarma, Roshan Kumar (2018), Data from: Experimental evolution demonstrates evolvability of preferential nutrient allocation to competing traits, in response to chronic malnutrition., Dryad, Dataset, https://doi.org/10.5061/dryad.60s6033

Abstract

Investigating the evolutionary origins of disease vulnerability is an important aspect of evolutionary medicine that strongly complements our current understanding on proximate causes of disease. Life history trade-offs mediated through evolutionary changes in resource allocation strategies could be one possible explanation to why suboptimal traits that leave bodies vulnerable to disease exist. For example, Drosophila melanogaster populations experimentally evolved to tolerate chronic larval malnutrition succumb to intestinal infection despite eliciting a competent immune response, owing to the loss of their intestinal integrity. Here, I test if evolved changes in resource allocation underlies this trade-off, by assaying preferential allocation of dietary protein towards growth and tissue repair in the same populations. Using two phenotypic traits: regeneration of intestinal epithelium post-pathogenic infection and body weight, I show that in accordance to the dynamic energy budget theory (DEB) dietary protein acquired during the larval phase is allocated to both growth and adult tissue repair. Furthermore, by altering the ratio of protein and carbohydrates in the larval diets I demonstrate that in comparison to the control populations, the evolved (selected) populations differ in their protein allocation strategy towards these two traits. While the control populations stored away excess protein for tissue repair, the selected populations invested it towards immediate increase in body weight rather than towards an unanticipated tissue damage. Thus, I show how macronutrient availability and their allocation between traits can alter resistance, and provide empirical evidence that supports the ‘mismatch hypothesis’, wherein vulnerability to disease is proposed to stem from the differences between ancestral and current environment.

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