Long-term social dynamics drive loss of function in pathogenic bacteria
Long-term social dynamics drive loss of function in pathogenic bacteria
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DOI：
10.1073/pnas.1508324112
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发表时间：
2015-08-25
影响因子：
11.1
通讯作者：
Griffin, Ashleigh S.
中科院分区：
文献类型：
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作者：
Andersen, Sandra Breum;Marvig, Rasmus Lykke;Griffin, Ashleigh S.
实验室实验表明，细菌细胞之间的社会相互作用可以推动种群水平的进化变化，但重大挑战限制了评估这些发现与自然种群相关性的尝试，其中选择压力是未知的。我们有越来越复杂的方法来监测引起传染病的细菌的表型和基因型动态，但相比之下，我们缺乏对这些变化的基于证据的适应性解释。感染过程中的进化变化通常被解释为宿主适应，但这种假设忽略了考虑体外驱动进化变化的社会动力学。我们提供的证据表明，在病原体中观察到的长期行为动力学是由选择驱动的，通过社会互动来胜过邻近的同种细胞。我们发现，铜绿假单胞菌，导致肺部感染的囊性纤维化患者，失去合作铁的收购铁载体生产过程中感染。这种损失可能是由肺中铁可用性的变化引起的，但令人惊讶的是，我们发现细胞保留了吸收同种产生的铁载体的能力，即使在它们失去合成铁载体的能力之后。只有当合作社生产者从人口中消失时，吸收的受体才会消失。这一发现强调了将致病细菌群体中的功能丧失解释为宿主环境中性状冗余的证据的潜在陷阱。更一般地说，我们提供了一个例子，序列分析可以用来产生可检验的假设选择驱动长期表型变化的病原菌在原位。
Laboratory experiments show that social interactions between bacterial cells can drive evolutionary change at the population level, but significant challenges limit attempts to assess the relevance of these findings to natural populations, where selection pressures are unknown. We have increasingly sophisticated methods for monitoring phenotypic and genotypic dynamics in bacteria causing infectious disease, but in contrast, we lack evidence-based adaptive explanations for those changes. Evolutionary change during infection is often interpreted as host adaptation, but this assumption neglects to consider social dynamics shown to drive evolutionary change in vitro. We provide evidence to show that long-term behavioral dynamics observed in a pathogen are driven by selection to outcompete neighboring conspecific cells through social interactions. We find that Pseudomonas aeruginosa bacteria, causing lung infections in patients with cystic fibrosis, lose cooperative iron acquisition by siderophore production during infection. This loss could be caused by changes in iron availability in the lung, but surprisingly, we find that cells retain the ability to take up siderophores produced by conspecifics, even after they have lost the ability to synthesize siderophores. Only when cooperative producers are lost from the population is the receptor for uptake lost. This finding highlights the potential pitfalls of interpreting loss of function in pathogenic bacterial populations as evidence for trait redundancy in the host environment. More generally, we provide an example of how sequence analysis can be used to generate testable hypotheses about selection driving long-term phenotypic changes of pathogenic bacteria in situ.