Abstract
ABSTRACTNumerous studies have shown that animal nutrition is tightly linked to gut microbiota, especially under nutritional stress. In Drosophila melanogaster, microbiota are known to promote juvenile growth, development, and survival on poor diets, mainly through enhanced digestion leading to changes in hormonal signaling. Here, we show that this reliance on microbiota is greatly reduced in replicated Drosophila populations that became genetically adapted to a poor larval diet in the course of over 170 generations of experimental evolution. Protein and polysaccharide digestion in these poor-diet-adapted populations became much less dependent on colonization with microbiota. This was accompanied by changes in expression levels of dFOXO transcription factor, a key regulator of cell growth and survival, and many of its targets. These evolutionary changes in the expression of dFOXO targets to a large degree mimic the response of the same genes to microbiota, suggesting that the evolutionary adaptation to poor diet acted on mechanisms that normally mediate the response to microbiota. Our study suggests that some metazoans have retained the evolutionary potential to adapt their physiology such that association with microbiota may become optional rather than essential.
Highlights
Numerous studies have shown that animal nutrition is tightly linked to gut microbiota, especially under nutritional stress
We performed 16S rRNA gene sequencing on larvae that were collected from their respective breeding diets
We set out to address the physiological bases of evolutionary adaptation to chronic nutritional stress, expecting that they would involve an improved ability of the animal host to exploit its microbiota
Summary
Numerous studies have shown that animal nutrition is tightly linked to gut microbiota, especially under nutritional stress. Microbiota may initially greatly facilitate coping with suboptimal diets, chronic nutritional stress experienced over multiple generations leads to evolutionary adaptation in physiology and gut digestive properties that reduces dependence on the microbiota for growth and survival. The same strain of L. plantarum that alleviates the effect of nutrient limitation on growth of mice [2] promotes the growth of Drosophila larvae on a protein-poor diet This effect is mediated through upregulation of the host’s proteolytic enzymes, leading to enhanced digestion and modulation of insulin and TOR pathways [6, 7]. Acetobacter pomorum, was found to promote Drosophila larval growth by modulating insulin/ IGF-like signaling (IIS); this phenotype was again pronounced on poor diets [8] Based on these findings, one might hypothesize that animal populations often exposed to chronic malnutrition would adapt by evolving an improved ability to benefit from their microbiota. This indicates that the site-specific function of dFOXO contributes to the physiological changes underpinning adaptation to nutritional stress, paralleling the microbiota effect in the nonadapted Control populations
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