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慢性营养应激适应导致. 减少对微生物组的依赖。

Adaptation to Chronic Nutritional Stress Leads to Reduced Dependence on Microbiota in .

机构信息

Department of Ecology and Evolution, University of Lausanne, Lausanne, Switzerland

Department of Fundamental Microbiology, University of Lausanne, Lausanne, Switzerland.

出版信息

mBio. 2017 Oct 24;8(5):e01496-17. doi: 10.1128/mBio.01496-17.

DOI:10.1128/mBio.01496-17
PMID:29066546
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5654931/
Abstract

Numerous studies have shown that animal nutrition is tightly linked to gut microbiota, especially under nutritional stress. In , 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 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. Animals depend on gut microbiota for various metabolic tasks, particularly under conditions of nutritional stress, a relationship usually regarded as an inherent aspect of animal physiology. Here, we use experimental evolution in fly populations to show that the degree of host dependence on microbiota can substantially and rapidly change as the host population evolves in response to poor diet. Our results suggest that, although 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. Thus, despite its ancient evolutionary history, the reliance of animal hosts on their microbial partners can be surprisingly flexible and may be relaxed by short-term evolution.

摘要

大量研究表明,动物营养与肠道微生物群密切相关,尤其是在营养压力下。众所周知,微生物群通过增强消化作用导致激素信号的变化,从而促进幼体在不良饮食下的生长、发育和存活。在这里,我们表明,在经过 170 多代实验进化后,对微生物群的这种依赖在大量复制的种群中大大减少,这些种群在遗传上适应了不良的幼虫饮食。在这些适应不良饮食的种群中,蛋白质和多糖的消化对微生物群的定植依赖性大大降低。这伴随着 dFOXO 转录因子表达水平的变化,dFOXO 转录因子是细胞生长和存活的关键调节因子,及其许多靶标。这些 dFOXO 靶基因表达的进化变化在很大程度上模拟了相同基因对微生物群的反应,这表明对不良饮食的进化适应作用于通常介导对微生物群反应的机制。我们的研究表明,一些后生动物保留了适应其生理机能的进化潜力,使得与微生物群的联系可能变得可选而不是必需。动物依赖肠道微生物群来完成各种代谢任务,尤其是在营养压力下,这种关系通常被认为是动物生理学的固有方面。在这里,我们使用果蝇种群的实验进化来表明,随着宿主种群对不良饮食的反应而进化,宿主对微生物群的依赖程度可以大大且迅速地改变。我们的研究结果表明,尽管微生物群最初可能极大地促进了对次优饮食的应对,但在多个世代中经历的慢性营养压力会导致生理学和肠道消化特性的进化适应,从而减少对微生物群的生长和存活的依赖。因此,尽管微生物群与动物宿主的联系具有古老的进化历史,但动物宿主对其微生物伙伴的依赖可能具有惊人的灵活性,并且可以通过短期进化来放松。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/5654931/11ab9d0687f8/mbo0051735420005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/5654931/639766fb1f7b/mbo0051735420001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/5654931/6b91bbc6cadb/mbo0051735420002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/5654931/3f0a488513d3/mbo0051735420003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/5654931/cffa47d04b98/mbo0051735420004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/5654931/11ab9d0687f8/mbo0051735420005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/5654931/639766fb1f7b/mbo0051735420001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/5654931/6b91bbc6cadb/mbo0051735420002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/5654931/3f0a488513d3/mbo0051735420003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/5654931/cffa47d04b98/mbo0051735420004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/5654931/11ab9d0687f8/mbo0051735420005.jpg

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