Verticillium alfalfae and V. dahliae, Agents of Verticillium Wilt Diseases

Verticillium dahliae and V. alfalfae (formerly Verticillium albo-atrum) are two important agricultural pathogens that affect many crops around the world and cause a distinct type of vascular wilt, which are known as Verticillium wilts. Several V. alfalfae and V. dahliae genomes have been sequenced, and are among the smaller genomes from filamentous ascomycetes. The number of predicted protein-encoding genes is similar to the saprobe Neurospora crassa. Perhaps reflective of their particular hemibiotrophic life styles, some gene families are expanded in the V. alfalfae and V. dahliae genomes. These include the gene families encoding glycoside hydrolases GH88, necrosis and ethylene-inducing-like proteins (NLPs), LysM effectors, proteins with chitin-recognition motifs, and cutinases. But the number of predicted secreted proteins was less than half that of the related Colletotrichum species, the agents of anthracnose diseases. V. dahliae strains generally contain lineage-specific regions (LS regions), which may play an important role in virulence and pathogenicity. Examples for horizontal transfer into Verticillium ancestors include the virulence factor Ave1, a glucan glucosyltransferase, and potentially some of the retrotransposons. The V. alfalfae and V. dahliae genomes have already had significant impacts on various aspects of basic and applied Verticillium research

Insights from the genome of the biotrophic fungal plant pathogen Ustilago maydis.

Ustilago maydis is a ubiquitous pathogen of maize and a well-established model organism for the study of plant-microbe interactions. This basidiomycete fungus does not use aggressive virulence strategies to kill its host. U. maydis belongs to the group of biotrophic parasites (the smuts) that depend on living tissue for proliferation and development. Here we report the genome sequence for a member of this economically important group of biotrophic fungi. The 20.5-million-base U. maydis genome assembly contains 6,902 predicted protein-encoding genes and lacks pathogenicity signatures found in the genomes of aggressive pathogenic fungi, for example a battery of cell-wall-degrading enzymes. However, we detected unexpected genomic features responsible for the pathogenicity of this organism. Specifically, we found 12 clusters of genes encoding small secreted proteins with unknown function. A significant fraction of these genes exists in small gene families. Expression analysis showed that most of the genes contained in these clusters are regulated together and induced in infected tissue. Deletion of individual clusters altered the virulence of U. maydis in five cases, ranging from a complete lack of symptoms to hypervirulence. Despite years of research into the mechanism of pathogenicity in U. maydis, no 'true' virulence factors had been previously identified. Thus, the discovery of the secreted protein gene clusters and the functional demonstration of their decisive role in the infection process illuminate previously unknown mechanisms of pathogenicity operating in biotrophic fungi. Genomic analysis is, similarly, likely to open up new avenues for the discovery of virulence determinants in other pathogens. ©2006 Nature Publishing Group