Genomic insights into Raffaelea lauricola pathogenesis

<p>Laurel wilt<span> caused by </span><i>Raffaelea lauricola</i> <span>is a lethal vascular disease of North </span>American members of the Lauraceae plant family. This fungus and its primary ambrosia beetle vector <i>Xyleborus glabratus </i>originated from Asia; however, there is no report of laurel wilt causing widespread mortality on native Lauraceae trees in Asia. To gain insight into why <i>R. lauricola</i> is a tree-killing plant pathogen in North America, we generated and compared high quality draft genome assemblies of <i>R. lauricola </i>and its closely related non-pathogenic species <i>R. aguacate. </i>Relative to <i>R. aguacate</i>, the <i>R. lauricola</i> genome uniquely encodes several small-secreted proteins that are associated with virulence in other pathogens and is enriched in secondary metabolite biosynthetic clusters, particularly polyketide synthase (PKS), non-ribosomal peptide synthetase (NRPS) and PKS-NRPS anchored gene clusters. The two species<i> </i>also exhibit significant differences in secreted proteins including CAZymes that are associated with polysaccharide binding including the chitin binding CBM50 (LysM) domain. Transcriptomic comparisons of inoculated redbay trees and <i>in vitro</i>-grown fungal cultures further revealed a number of secreted protein genes, secondary metabolite clusters and alternative sulfur uptake and assimilation pathways that are coordinately up-regulated during infection. Through these comparative analyses we have identified potential adaptations of <i>R. lauricola</i> that may enable it to colonize and cause disease on susceptible hosts. How these adaptations have interacted with co-evolved hosts in Asia, where little to no disease occurs, and non-co-evolved hosts in North America, where lethal wilt occurs, requires additional functional analysis of genes and pathways.</p>