SPP 1819: Rapid evolutionary adaptation: Potential and constraints

描述了几种快速进化的情景，但最突出的一个是物种在寄生或病原相互作用中的适应。许多活体营养型病原体具有高度的宿主特异性，这通常与相互作用的种群中的战壕战或军备竞赛动态有关。近年来在植物-病原系统中发现了多种毒力因子，但其寄主特异性的遗传机制及其进化至今仍不清楚。传统上，基因对基因模型已被送达解释主机的特异性和协同进化，但只有少数模型系统似乎依赖于无毒和抗性基因的这种相互作用。因此，在大多数模式系统中，宿主特异性和快速适应新宿主的机制是未知的。近年来，杂交的相关性，以克服进化的死胡同的情况下，主机特异性变得流行和几个人口的研究集中在渐渗杂交，以解释主机跳跃或主机开关。然而，这些研究使用了基于群体遗传学的方法，并没有分析杂交的机制到目前为止，在这里，我们建议使用实验进化的模式系统微孢霉-Silene产生杂交种的相关物种和选择后，新的主机主机上的主机跳跃的菌株。初步研究表明，杂交感染以合理的频率发生，甚至与亲本菌株回交也会导致阳性感染，并获得对新宿主的致病性。后代的比较基因组学揭示了大多数染色体上频繁的重组事件。我们建议将实验进化扩展到F3回交，并对每一代的代表性菌株进行相关数量的测序，以比较父母，杂交种和回交的基因组内容和组织。这将允许鉴定与宿主特异性相关的候选基因座。此外，我们计划分析兼容和不兼容的宿主-病原体相互作用的转录组，以验证候选基因，并分析它们在宿主特异性感染过程中的作用。转录组方法还可以区分通过调节元件重组获得的剂量效应和由单个基因控制的适应性效应。因此，我们的项目旨在更好地了解通过杂交宿主跳跃的快速进化。

Several scenarios of rapid evolution are described, but one of the most prominent is the adaptation of species in parasitic or pathogenic interactions. Many biotrophic pathogens are highly host specific, which is often discussed with respect to trench warfare or arms race dynamics in the interacting populations. Several virulence factors have been identified in the last years in various plant-pathogen systems, but the genetic mechanism of host specificity and its evolution remains unclear up to date. Traditionally, gene-for-gene models have been served to explain host specificity and coevolution, but only few model systems seem to rely on such a reciprocal interaction of avirulence and resistance genes. Thus, the mechanisms of host specificity and rapid adaption to new hosts as needed for host jumps are unknown in most model systems. In recent years the relevance of hybridization to overcome an evolutionary dead-end situation of host specificity became popular and several populations studies focused on introgressive hybridization to explain host jumps or host switches. However, these studies used an approach based on population genetics and did not analyse the mechanisms of hybridization so far.Here we propose to use experimental evolution in the model system Microbotryum–Silene to produce hybrids of related species and select for strains after host jumps on new hosts. Preliminary studies showed, that hybrid infections occur at reasonable frequencies and even backcrosses with the parental strains result in positive infections and gained pathogenicity with respect to new hosts. Comparative genomics of the offspring reveals frequent recombination events on most chromosomes. We propose to extend the experimental evolution using hybrids into F3 backcrosses and to sequence a relevant number of representative strains of each generation to compare the genome content and organisation in parents, hybrids and backcrosses. This will allow identifying candidate loci relevant for host specificity. In addition, we plan to analyse the transcriptome of compatible and incompatible host-pathogen interactions, to validate the candidate genes and to analyse their role during host specific infection. The transcriptome approach would also allow differentiating between dosage effects gained through recombination in regulatory elements and fitness effects governed by individual genes. Thus, our project aims for a better understanding of the rapid evolution of host jumps through hybridization.