Beyond the Red Queen: are elevated parasite evolutionary rates driven by host shifts?

进化是随着时间的推移而变化的。大多数人都知道进化是对人为影响的反应--细菌进化出对抗生素的抗药性;工业污染导致了胡椒蛾的黑暗形式的进化。然而，在自然系统中，进化最快的是那些有助于寄生虫感染性和它们感染的生物体阻止寄生虫繁殖的能力的基因。40年前，利·货车·瓦伦提出了一个理论，解释了为什么与寄生虫感染性和宿主抗性有关的基因进化得比其他基因更快。这一理论指出，在“相互对抗”的情况下，进化将是迅速的。寄生虫进化以抵抗寄生虫的感染，因此寄生虫必须适应以绕过这种抵抗（或死亡）。反过来，当寄生虫适应更好地感染宿主时，宿主也必须适应（或死亡）。这创造了一个被称为拮抗共同进化的连续循环，其中寄生虫毒力和宿主防御基因在军备竞赛中不断适应和反适应。宿主和寄生虫之间这种持续的“追赶”与刘易斯卡罗尔的名著《镜中奇遇》中的一个场景相似，在这本书中，爱丽丝（又名爱丽丝）爱丽丝梦游仙境）运行迅速与邪恶的红皇后，但无处可去。红皇后相互作用被广泛认为是参与宿主防御和寄生虫毒力的基因迅速进化的原因。然而，这可能只是一个部分的错误。该提案旨在测试一种迄今为止很少研究的寄生虫基因快速进化的替代解释：寄生虫毒力基因快速进化是因为寄生虫偶尔会转换宿主物种。宿主转换在寄生虫中很常见。我们都听说过它-艾滋病毒从灵长类动物转移到人类大约70年前，猪流感和禽流感已经提高了我们对新流感从猪和鸟类转移到人类的认识。很可能寄生虫的宿主转换代表了一种非常强的选择力。宿主转换后，寄生虫的整个环境都不同了，寄生虫在新宿主中的表现可能很差。因此，寄生虫有很大的适应新宿主的余地，它必须迅速进化以更好地利用宿主。很明显，寄生虫确实经常“转换”宿主，而且很可能伴随着一轮强烈的自然选择，这可以解释为什么寄生虫的“毒力”基因进化得很快。在这个项目中，我们将测试宿主转移驱动寄生虫快速进化的理论。在实验室中，我们将为细菌产生宿主转移事件，将细菌从其原生宿主转移到新的“外来”宿主中。我们将把这种细菌留在新的宿主物种中一年，然后再把它找回来，我们将调查宿主的转移是否导致细菌在基因序列方面进化得更快，以及它在新宿主中繁殖的能力是否得到了进化。我们还将研究细菌在宿主物种中的多样性，这些物种通过自然界中的宿主转换而定殖。通过比较野生细菌菌株与实验室宿主转移后的细菌菌株之间的差异，我们可以询问自然多样性是否可能是由过去遇到的宿主转移事件驱动的

Evolution is change over time. Most people know of evolution in terms of responses to man-made influences - bacteria evolve resistance to antibiotics; industrial pollution led to the evolution of dark forms of the peppered moth. However, in natural systems, evolution is most rapid in genes that contribute to parasite infectivity and to the ability of the organisms they infect to stop parasites from propagating. Forty years ago, Leigh Van Valen produced a theory as to why genes involved in parasite infectivity and host resistance should evolve more quickly than others. This theory noticed that evolution would be rapid where there was 'mutual antagonism'. Hosts evolve to resist infection by parasites, so parasites must adapt to circumvent this resistance (or die). Reciprocally, as the parasites adapt to better infect their hosts, so the hosts must adapt (or die). This creates a continual cycle termed antagonistic coevolution, where parasite virulence and host defence genes continually adapt, and counter adapt, in an arms race. This continuous 'catch up' between hosts and parasites parallels a scene from Lewis Carrol's famous book, Through the Looking Glass, in which Alice (a.k.a. Alice in Wonderland) runs rapidly with the evil Red Queen, yet gets nowhere. Red Queen interactions are widely accepted as 'the' reason why genes involved in host defence and parasite virulence evolve quickly. However, it is possible that it is only a partial explanaiton. This proposal seeks to test an alternative explanation for fast evolution of parasite genes rarely examined to date: parasite virulence genes evolve rapidly because parasites occasionally switch host species. Host switching occurs quite commonly in parasites. We have all heard about it- HIV moved from primates into humans about 70 years ago, and Swine Flu and Avian flu have raised our awareness of new influenza shifting from pigs and birds into humans. It is likely that host switching by a parasite represents a very strong selective force. Following a host switch, the entire environment of the parasite is different, and a parasite in its new host is likely to perform poorly. Thus, there is great scope for adaptation of the parasite to its new host, and it must rapidly evolve to better exploit the host. It is clear that parasites do 'switch' hosts quite commonly, and very likely this is accompanied by a bout of strong natural selection that may explain why parasite 'virulence' genes evolve rapidly. In this project, we will test the theory that host shifts drive fast parasite evolution. In the laboratory, we will produce host shift events for a bacterium, moving the bacterium from its native host into a new 'foreign' one. We will leave this bacterium in its new host species for a year, and then recover it. We will investigate whether the host shift has resulted in the bacterium evolving more quickly in terms of gene sequence, and whether it has evolved in terms of its ability to prosper in its new host. We will also examine the diversity of the bacterium across host species which it has colonised through host switching in nature. By comparing the differences seen between bacterial strains in the wild to those following laboratory host shifts, we can ask if natural diversity is likely driven by the host shift events it has encountered in the past