Abstract
Fusarium graminearum is an opportunistic pathogen of cereals where it causes severe yield losses and concomitant mycotoxin contamination of the grains. The pathogen has mixed biotrophic and necrotrophic (saprophytic) growth phases during infection and the regulatory networks associated with these phases have so far always been analyzed together. In this study we compared the transcriptomes of fungal cells infecting a living, actively defending plant representing the mixed live style (pathogenic growth on living flowering wheat heads) to the response of the fungus infecting identical, but dead plant tissues (cold-killed flowering wheat heads) representing strictly saprophytic conditions. We found that the living plant actively suppressed fungal growth and promoted much higher toxin production in comparison to the identical plant tissue without metabolism suggesting that molecules signaling secondary metabolite induction are not pre-existing or not stable in the plant in sufficient amounts before infection. Differential gene expression analysis was used to define gene sets responding to the active or the passive plant as main impact factor and driver for gene expression. We correlated our results to the published F. graminearum transcriptomes, proteomes, and secretomes and found that only a limited number of in planta- expressed genes require the living plant for induction but the majority uses simply the plant tissue as signal. Many secondary metabolite (SM) gene clusters show a heterogeneous expression pattern within the cluster indicating that different genetic or epigenetic signals govern the expression of individual genes within a physically linked cluster. Our bioinformatic approach also identified fungal genes which were actively repressed by signals derived from the active plant and may thus represent direct targets of the plant defense against the invading pathogen.
Highlights
Fusarium graminearum is a plant pathogenic ascomycete fungus causing various plant diseases on small-grain cereals such as Fusarium head blight (FHB or scrab) of wheat (Triticium aestivum) and barley (Hordeum vulgare) as well as ear and stalk rot of maize (Zea mays; McMullen et al, 1997; Bottalico and Perrone, 2002; Stack, 2003; Goswami and Kistler, 2004)
This condition is subsequently referred to as “pathogenic growth.”. Another set of three ears, which were cut off the plant and shockfrozen in liquid nitrogen prior to spore application, was identically inoculated representing the same plant substrate but without active metabolism and defense responses
The aim of our study was to better define the group of “in planta” expressed fungal genes because the pathogenic growth status represents a mixture of genes responding to the plant tissue as substrate already present as well as genes responding to defense signals and metabolites built up in response to the pathogenic attack
Summary
Fusarium graminearum (telemorph: Giberella zeae) is a plant pathogenic ascomycete fungus causing various plant diseases on small-grain cereals such as Fusarium head blight (FHB or scrab) of wheat (Triticium aestivum) and barley (Hordeum vulgare) as well as ear and stalk rot of maize (Zea mays; McMullen et al, 1997; Bottalico and Perrone, 2002; Stack, 2003; Goswami and Kistler, 2004). The infection process is accompanied by the formation of infection cushions (Boenisch and Schäfer, 2011), an agglomeration of fungal hyphae which secrete various hydrolyzing enzymes able to degrade components of the epidermal plant cuticle and the plant cell wall, such as e.g., cutinases, pectinases, hemicellulases, cellulases, and lipases (Kang and Buchenauer, 2000; Bushnell et al, 2003; Voigt et al, 2005; Cuomo et al, 2007; Walter et al, 2010) After this initial stage of surface colonization (between the time span of roughly 20 and 70 h after infection, abbreviated hai), asymptotic intercellular fungal growth occurs, which resembles the lifestyle of biotrophic fungi. G protein- coupled receptors have been reported to be involved in host recognition followed by downstream signaling cascades involving the mitogen-activated protein kinases (MAPK) FgGPMK1 (Jenczmionka et al, 2003; Jenczmionka and Schafer, 2005) and FgMGV1 (Hou et al, 2002) as well as the heterotrimeric G protein subunits Gα (GzGPA1, 2, and 3), Gβ (GzGPB1), Gγ (GzGPG1), and the Ras-GTPase RAS2
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