SPP 1819: Rapid evolutionary adaptation: Potential and constraints

描述了几种快速进化的情况，但其中最突出的是物种在寄生或致病性相互作用中的适应。许多生物营养病原体具有高度的宿主特异性，这通常与相互作用种群中的堑壕战或军备竞赛动力学有关。近年来，在各种植物-病原体系统中已经发现了几种毒力因子，但宿主特异性的遗传机制及其进化至今仍不清楚。传统上，基因换基因模型已经被用来解释宿主特异性和共同进化，但只有少数模型系统似乎依赖于这种无毒基因和抗性基因的相互作用。因此，在大多数模型系统中，宿主特异性和宿主跳跃所需的对新宿主的快速适应机制尚不清楚。近年来，杂交与克服宿主特异性的进化死胡同的相关性变得流行起来，一些种群研究集中在渐进杂交上，以解释宿主跳跃或宿主切换。然而，这些研究采用的是基于群体遗传学的方法，尚未对杂交机制进行分析。在此，我们建议在Microbotryum-Silene模型系统中使用实验进化来产生相关物种的杂交，并在宿主跳到新宿主后选择菌株。初步研究表明，杂交感染发生在合理的频率，甚至与亲本株回交导致阳性感染，并获得了对新宿主的致病性。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。我们建议将使用杂交的实验进化扩展到F3回交，并对每一代的相关数量的代表性菌株进行测序，以比较亲本、杂交和回交的基因组内容和组织。这将有助于识别与宿主特异性相关的候选基因座。此外，我们计划分析相容和不相容宿主-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中的作用。转录组方法还可以区分通过重组调控元件获得的剂量效应和由单个基因控制的适应度效应。因此，我们的项目旨在通过杂交更好地理解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.