alterations in and their effects on DMI sensitivity and fitness.

Unlabelled: the causal agent of early blight, may dramatically reduce yield in potato production on a global scale. Quinone outside inhibitors (QoIs), succinate dehydrogenase inhibitors (SDHIs), and demethylation inhibitors (DMIs) represent three major fungicide groups that are used to control early blight on potato. Early blight has acquired adaptation to QoIs and SDHIs, making DMI fungicides the prime class of chemistries in early blight control.

The serine-threonine protein kinase Snf1 orchestrates the expression of plant cell wall-degrading enzymes and is required for full virulence of the maize pathogen Colletotrichum graminicola.

Colletotrichum graminicola, the causal agent of maize leaf anthracnose and stalk rot, differentiates a pressurized infection cell called an appressorium in order to invade the epidermal cell, and subsequently forms biotrophic and necrotrophic hyphae to colonize the host tissue. While the role of force in appressorial penetration is established (Bechinger et al., 1999), the involvement of cell wall-degrading enzymes (CWDEs) in this process and in tissue colonization is poorly understood, due to the enormous number and functional redundancy of these enzymes.

The Small Ras Superfamily GTPase Rho4 of the Maize Anthracnose Fungus Is Required for β-1,3-glucan Synthesis, Cell Wall Integrity, and Full Virulence.

Small Ras superfamily GTPases are highly conserved regulatory factors of fungal cell wall biosynthesis and morphogenesis. Previous experiments have shown that the Rho4-like protein of the maize anthracnose fungus , formerly erroneously annotated as a Rho1 protein, physically interacts with the β-1,3-glucan synthase Gls1 (Lange et al., 2014; Curr.

Fungal Pathogenesis-Related Cell Wall Biogenesis, with Emphasis on the Maize Anthracnose Fungus .

The genus harbors many plant pathogenic species, several of which cause significant yield losses in the field and post harvest. Typically, in order to infect their host plants, spores germinate, differentiate a pressurized infection cell, and display a hemibiotrophic lifestyle after plant invasion. Several factors required for virulence or pathogenicity have been identified in different species, and adaptation of cell wall biogenesis to distinct stages of pathogenesis has been identified as a major pre-requisite for the establishment of a compatible parasitic fungus-plant interaction.

Molecular Characterization of the Purine Degradation Pathway Genes and of the Maize Anthracnose Fungus Identified Urease as a Novel Target for Plant Disease Control.

Fungal pathogenicity is governed by environmental factors, with nitrogen playing a key role in triggering pathogenic development. Spores germinating on the plant cuticle are exposed to a nitrogen-free environment, and reprograming of nitrogen metabolism is required for bridging the time needed to gain access to the nitrogen sources of the host. Although degradation of endogenous purine bases efficiently generates ammonium and may allow the fungus to bridge the preinvasion nitrogen gap, the roles of the purine degradation pathway and of the key genes encoding allantoicase and urease are largely unknown in plant pathogenic fungi.