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。大多数人知道进化是根据对人为影响的反应来理解的--细菌对抗生素产生抗药性；工业污染导致胡椒蛾黑色形态的进化。然而，在自然系统中，导致寄生虫传染性和它们感染的有机体阻止寄生虫繁殖的基因进化最快。40年前，利·范·瓦伦提出了一种理论，解释了为什么参与寄生虫传染性和宿主抗性的基因进化应该比其他基因进化得更快。这一理论注意到，在“相互对立”的地方，进化将是快速的。宿主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(否则就会死亡)。反过来，随着寄生虫适应更好地感染它们的宿主，宿主也必须适应(或死亡)。这创造了一种被称为对抗性共同进化的连续循环，在这种循环中，寄生虫的毒力和宿主防御基因在军备竞赛中不断适应和反适应。寄主和寄生虫之间的这种持续的追赶与刘易斯·卡罗尔的名著《透过镜子》中的一个场景相似，在这本书中，爱丽丝(又名。《爱丽丝梦游仙境》)与邪恶的红皇后一起快速奔跑，但一无所获。红皇后的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进化迅速的原因。然而，它可能只是一个部分的解释。这一提议旨在测试另一种对寄生虫基因快速进化的解释：寄生虫毒力基因之所以进化迅速，是因为寄生虫偶尔会更换宿主物种。寄主切换在寄生虫中很常见。我们都听说过这件事--大约70年前，艾滋病毒从灵长类动物传播到人类，而猪流感和禽流感提高了我们对新流感从猪和鸟传播到人类的认识。寄生虫的宿主转换很可能代表了一种非常强的选择性力量。在宿主切换之后，寄生虫的整个环境是不同的，寄生虫在新宿主中的表现可能会很差。因此，寄生虫有很大的适应新宿主的空间，它必须迅速进化，以更好地利用宿主。很明显，寄生虫确实很常见地“交换”宿主，很可能伴随着一轮强大的自然选择，这可能解释了为什么寄生虫的“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，将细菌从其本地宿主转移到新的“外来”宿主。我们将把这种细菌放在它的新宿主物种中一年，然后再回收它。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，以及它是否在新宿主中繁荣的能力方面进化。我们还将检查细菌在寄主物种中的多样性，这些寄主物种是通过在自然界中切换宿主而定植的。通过比较野生细菌菌株与实验室宿主转移后的菌株之间的差异，我们可以问，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