Experimental host-parasite coevolution in a changing environment

理论预测，应激源可以对宿主-寄生虫相互作用产生多重影响，要么增加抵抗力下降的宿主数量，要么减少宿主丰度，从而降低寄生虫的传播率。同样地，压力可以促进寄生虫毒力或致病性的增加或减少。草履虫/ Caedibacter宿主-寄生虫系统的所谓杀伤特性将用于研究这些悬而未决的问题。四虫草履虫的这种杀伤特性是由垂直传播的细菌寄生虫带螺旋Caedibacter taeniospiralis介导的，它为其宿主提供了选择性竞争优势。受感染的草履虫向培养基中释放少量的寄生虫。在被无寄生虫的草履虫摄入后，细菌杀伤毒素杀死宿主的易感竞争者。因此，在这个系统中，寄生虫可以朝着增加或减少致病性的方向进化。我们建议分析热应激下长期实验共同进化的结果。特别是，我们将研究应激增加寄生虫致病性的假设，这同时促进草履虫对杀伤毒素抗性的进化。此外，我们将验证宿主的快速进化是基于表观遗传变化的假设，以及对杀伤毒素的抗性是基因型特异性的假设。将采用实验和分子相结合的方法来了解草履虫在基因组水平上的杀伤毒素抗性进化以及寄生虫致病性的功能背景。

Theory predicts that stressors can have multiple effects on a host-parasite interaction either by increasing the number of hosts with decreased resistance or by reducing host abundance and consequently the transmission rate of the parasite. Likewise, stress can promote an increase or decrease of parasite virulence or pathogenicity. The so-called killer trait of the Paramecium / Caedibacter host-parasite system will be used to investigate these open questions. This killer trait of Paramecium tetraurelia is mediated by the vertically transmitted bacterial parasite Caedibacter taeniospiralis, which offers a selective competition advantage to its host. Infected paramecia release low amounts of their parasite into the medium. After ingestion by a parasite-free Paramecium, the bacterial killer-toxin kills the susceptible competitor of the host. Consequently, in this system the parasite can evolve towards increased or decreased pathogenicity. We propose to analyse the outcome of a long-term experimental co-evolution under heat stress. Particularly, we will investigate the hypothesis that stress increases parasite pathogenicity, which concomitantly fosters the evolution of a killer-toxin resistance in Paramecium. Further, we will test the hypothesis that the rapid evolution of the host is based on epigenetic changes and that the killer-toxin resistance is genotype specific. Combined experimental and molecular approaches will be used to understand the evolution of Paramecium’s killer-toxin resistance at a genomic level as well as the functional background of parasite pathogenicity.