SPP 1819: Rapid evolutionary adaptation: Potential and constraints

Basic data for this project

Description

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.