Experimental Evolution of Metabolic Dependency in Bacteria

Experimental Evolution of Metabolic Dependency in Bacteria
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DOI:
10.1371/journal.pgen.1006364
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发表时间:
2016-11-01
期刊:
影响因子:
4.5
通讯作者:
Kost, Christian
Kost, Christian
中科院分区:
生物学2区
文献类型:
--
作者:
D'Souza, Glen;Kost, Christian

文献摘要

被引文献

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细菌经常丢失生物合成基因,从而使它们依赖于相应代谢物的环境吸收。尽管这种“基因组流线型”的普遍存在,但通常不清楚伴随的生物合成功能的丧失是自然选择的结果,还是随机遗传漂变造成的。在这里,我们通过实验证明,当相应的代谢物可以从环境中获得时,代谢功能的丧失是强烈选择的。在含氨基酸的环境中连续繁殖大肠杆菌的重复种群,发现营养缺陷型基因型在几乎所有重复种群中在不到2,000代的时间内迅速进化。此外,营养缺陷型也在缺乏氨基酸的环境中进化,但程度要小得多。这些生物合成功能的丧失是由于结构和调控基因的突变。在竞争实验中进行的氨基酸的存在下,营养缺陷型突变体获得了显着的健身优势的进化祖先,这表明他们的出现是有选择性的青睐。有趣的是,营养缺陷型突变体不仅通过环境摄取获得氨基酸,还通过共存菌株的交叉喂养获得氨基酸。我们的研究结果表明,适应性健身的好处可以有利于生物合成功能丧失突变体,并推动建立复杂的代谢相互作用的微生物群落。
Bacteria frequently lose biosynthetic genes, thus making them dependent on an environmental uptake of the corresponding metabolite. Despite the ubiquity of this 'genome streamlining', it is generally unclear whether the concomitant loss of biosynthetic functions is favored by natural selection or rather caused by random genetic drift. Here we demonstrate experimentally that a loss of metabolic functions is strongly selected for when the corresponding metabolites can be derived from the environment. Serially propagating replicate populations of the bacterium Escherichia coli in amino acid-containing environments revealed that auxotrophic genotypes rapidly evolved in less than 2,000 generations in almost all replicate populations. Moreover, auxotrophs also evolved in environments lacking amino acids-yet to a much lesser extent. Loss of these biosynthetic functions was due to mutations in both structural and regulatory genes. In competition experiments performed in the presence of amino acids, auxotrophic mutants gained a significant fitness advantage over the evolutionary ancestor, suggesting their emergence was selectively favored. Interestingly, auxotrophic mutants derived amino acids not only via an environmental uptake, but also by cross-feeding from coexisting strains. Our results show that adaptive fitness benefits can favor biosynthetic loss-of-function mutants and drive the establishment of intricate metabolic interactions within microbial communities.