Goal
Plants can be colonised by a broad range of microorganisms, ranging from prokaryotes to fungi and oomycetes. Notably, the two partners in these interactions (plant and microbe) are both subject to rapid adaptation by fast evolution. In nature, this is exemplified by the constant emergence of new resistance specificities on the host side and new virulence determinants on the pathogen side. However, the molecular mechanisms underlying these rapid adaptations are poorly understood.
This workshop will bring together a selection of internationally renowned experts working on both the host and the pathogen side to discuss the spectrum of molecular events that can lead to rapid adaptation by (co-)evolution of the respective interaction partners.
The expertise of the proposed scientists covers molecular evolution, evolution theory, molecular phytopathology and microbial pathogenomics. The workshop is meant to integrate a core group of researchers already collaborating within a priority program funded by the German Research Foundation (DFG; priority program 'SPP1819: Rapid evolutionary adaptation – potential and constraints') with a wide range of international scientists with similar research interests.
Rationale and scope
Host-parasite interactions are profound drivers of rapid evolutionary adaptations. The co-evolution between host and parasite exerts strong reciprocal genetic pressures that lead to fast mutual adaptation. This scenario gives rise to an evolutionary arms race that has been also conceptualized by the co-called “Red Queen Hypothesis”. Evolutionary adaptations are particularly fast in the context of host-parasite relationships especially when the interaction depends on just one or a few genes on the host or pathogen side. Evidence of such a scenario are highly co-evolved plant-pathogen interactions whose outcome is often dependent on classical gene-for-gene relationships. In these cases, the interaction between host and parasite are governed by corresponding pairs of resistance (R) and avirulence (Avr) genes. Avr genes typically encode pathogen effector proteins for host manipulation and defense suppression, while the cognate R genes code for (mostly cytoplasmic) receptors that recognize either the Avr protein itself or, alternatively, its biochemical activity (guard hypothesis). Matching R-Avr gene pairs are typically highly co-evolved and, because of adaptive evolution, often show extensive genetic variation within as well as between host and pathogen populations.
In many cases subtle genetic changes (point mutations) in either the R or Avr gene can give rise to dramatic alterations at the phenotypic level, exemplified as changes from virulence to avirulence or vice versa. Apart from these rather simple scenarios, virulence as well as resistance profiles can be likely modified by a range of further molecular mechanisms such as copy number variation, the activity of small regulatory RNAs and presence/absence of dispensable pathogen chromosomes, to name a few. The actual contribution of these features/mechanisms to the evolution of particular plant-microbe interactions remains, however, largely obscure. The advent of new DNA sequencing technologies now enables to trace these molecular events precisely at scales ranging from individuals to entire populations. This workshop is meant to discuss the molecular principles underlying rapid evolution in the light of various plant-microbe interactions, taking into account the benefits but also limitations of these new technologies. Another key aspect is to debate to which extent experimental evolution can help to unravel the underlying molecular forces.
Organising committee
Ralph Panstruga (RWTH Aachen University, Germany)
Laura Rose (Düsseldorf University, Germany)