Specialized infection strategies of falcate and oval conidia of Colletotrichum graminicola.

For many filamentous fungi with pathogenic lifestyles, the presence of distinct asexual conidia has been described. However, the role of these spore types remains mostly obscure. Colletotrichum graminicola is a hemibiotrophic filamentous fungus, causing anthracnose on maize plants with a high potential of epidemic disease spreading. C. graminicola generates two types of conidia. Falcate shaped conidia formed in necrotic lesions on maize tissues are able to generate appressoria with high efficiency and are considered key disease spreading propagules. The second conidia type, the smaller oval conidia, is formed in the vascular system of the infected plant, probably causing the distribution of the disease in planta. Barely any knowledge exists about how these conidia are able to exhibit their specific functions in the life cycle and pathogenicity of C. graminicola. Here, we show that germlings derived from both falcate and oval conidia differ in the secretion of a germination inhibitor and signals for germling fusion. Germination experiments combined with HPLC and mass spectrometry analyses revealed that germination of falcate conidia is regulated by the self-inhibitor mycosporine-glutamine, whereas this compound is absent from oval conidia cultures. Additionally, germlings derived from oval conidia undergo germling fusions at high frequencies and are able to induce such a fusion when co-incubated with falcate conidia. Falcate conidia germlings alone, however, were never observed to fuse. Plant infection experiments showed a positive correlation between germling fusions and efficient leaf infection by oval conidia. However, this correlation was not observed for infection by falcate conidia. Together, our findings reveal significant differences of two types of conidia derived from the same pathogenic fungus with distinct roles in pathogenesis.

Secondary metabolites of Hülle cells mediate protection of fungal reproductive and overwintering structures against fungivorous animals.

Fungal Hülle cells with nuclear storage and developmental backup functions are reminiscent of multipotent stem cells. In the soil, Hülle cells nurse the overwintering fruiting bodies of Aspergillus nidulans. The genome of A. nidulans harbors genes for the biosynthesis of xanthones. We show that enzymes and metabolites of this biosynthetic pathway accumulate in Hülle cells under the control of the regulatory velvet complex, which coordinates development and secondary metabolism. Deletion strains blocked in the conversion of anthraquinones to xanthones accumulate emodins and are delayed in maturation and growth of fruiting bodies. Emodin represses fruiting body and resting structure formation in other fungi. Xanthones are not required for sexual development but exert antifeedant effects on fungivorous animals such as springtails and woodlice. Our findings reveal a novel role of Hülle cells in establishing secure niches for A. nidulans by accumulating metabolites with antifeedant activity that protect reproductive structures from animal predators.

The Plasma Membrane: A Platform for Intra- and Intercellular Redox Signaling.

Membranes are of outmost importance to allow for specific signal transduction due to their ability to localize, amplify, and direct signals. However, due to the double-edged nature of reactive oxygen species (ROS)-toxic at high concentrations but essential signal molecules-subcellular localization of ROS-producing systems to the plasma membrane has been traditionally regarded as a protective strategy to defend cells from unwanted side-effects. Nevertheless, specialized regions, such as lipid rafts and caveolae, house and regulate the activated/inhibited states of important ROS-producing systems and concentrate redox targets, demonstrating that plasma membrane functions may go beyond acting as a securing lipid barrier. This is nicely evinced by nicotinamide adenine dinucleotide phosphate (NADPH)-oxidases (NOX), enzymes whose primary function is to generate ROS and which have been shown to reside in specific lipid compartments. In addition, membrane-inserted bidirectional H2O2-transporters modulate their conductance precisely during the passage of the molecules through the lipid bilayer, ensuring time-scaled delivery of the signal. This review aims to summarize current evidence supporting the role of the plasma membrane as an organizing center that serves as a platform for redox signal transmission, particularly NOX-driven, providing specificity at the same time that limits undesirable oxidative damage in case of malfunction. As an example of malfunction, we explore several pathological situations in which an inflammatory component is present, such as inflammatory bowel disease and neurodegenerative disorders, to illustrate how dysregulation of plasma-membrane-localized redox signaling impacts normal cell physiology.