The tomato immune receptor Ve1 governs resistance to race 1 strains of Verticillium, while race 2 strains are not recognized. Until recently, the Verticillium effector that is detected by Ve1 remained unknown. By high-throughput population genome sequencing, the gene that encodes the Ave1 effector (for Avirulence on Ve1 tomato) was identified. Interestingly, Ave1 homologs were also found in the fungal pathogens Cercospora beticola, Colletotrichum higginsianum and Fusarium oxysporum f. sp. lycopersici, some of which are recognized by Ve1. Based on the differential recognition of the Ave1 homologs, the epitope of the Ave1 protein has been identified. The identification of Ave1 facilitates functional analysis of the Ve1 immune receptor. Strictly asexual microorganisms, such as V. dahliae, are often considered as evolutionary dead ends as it remains unknown how they can generate the genetic variation that is required for coevolution with their hosts. Based on comparative population genomics we show that extensive chromosomal rearrangements establish highly dynamic ‘plastic’ genomic regions that act as a source for genetic variation to mediate aggressiveness and that are enriched for in planta-expressed effector genes. We propose that V. dahliae evolves by prompting chromosomal rearrangements, enabling rapid development of novel effector genes.
|Title of host publication||Book of Abstracts 11th International Verticillium Symposium, Göttingen, Germany, 5-8 May 2013|
|Publication status||Published - 2013|
|Event||11th International Verticillium Symposium, Göttingen, Germany - |
Duration: 5 May 2013 → 8 May 2013
|Conference||11th International Verticillium Symposium, Göttingen, Germany|
|Period||5/05/13 → 8/05/13|