Verticillium dahliae, causal agent of vascular wilt disease, is one of the most notorious plant pathogens of tomato. By comparative population genomics, we previously identified the race 1 specific effector that activates tomato immunity mediated by the cell surface receptor Ve1. Further comparative genomics revealed extensive genomic rearrangements between individual V. dahliae isolates that could be implicated in the occurrence of lineage-specific regions involved in niche adaptation and virulence. Remarkably, genes that reside in lineage-specific regions are over-represented during in planta expression. Moreover, in contrast to candidate effector genes that reside in the core genome, targeted disruption of several lineage-specific effector genes resulted in compromised virulence. One of the lineage-specific effectors that could be implicated in virulence on tomato is a LysM effector, a homolog of the Ecp6 effector of the foliar tomato pathogen Cladosporium fulvum that functions in suppression of chitin-triggered host immunity. Structural analysis revealed a novel mechanism for chitin binding by Ecp6 through intrachain LysM dimerization, leading to a composite binding site that binds chitin with ultra-high affinity.
Considering the importance of lineage-specific regions for V. dahliae aggressiveness, detailed genomic information on the recombination sites is required to understand how lineage-specific regions arise. To this end, we re-sequenced a V. dahliae genome with PacBio technology, leading to a gapless assembly of eight complete chromosomes. Our efforts to identify genomic signatures at the recombination sites and the molecular mechanism(s) that establish chromosomal rearrangements will be discussed.
|Conference||COST 2014 - 2nd Annual Conference of the SUSTAIN Action, Zakopane, Poland|
|Period||15/10/14 → 17/10/14|