Metabolic profiling of wheat rachis node infection by Fusarium graminearum – decoding deoxynivalenol‐dependent susceptibility

Abstract

Fusarium graminearum is a filamentous ascomycete and the causal agent of Fusarium head blight on wheat that threatens food and feed production worldwide as infection reduces crop yield both quantitatively by interfering with kernel development and qualitatively by poisoning any remaining kernels with mycotoxins. In wheat, F. graminearum infects spikelets and colonizes the entire head by growing through the rachis node at the bottom of each spikelet. Without the mycotoxin deoxynivalenol (DON), the pathogen cannot penetrate the rachis node and wheat is able to resist colonization. Using a global metabolite profiling approach we compared the metabolic profile of rachis nodes inoculated with either water, the Fusarium graminearum wild-type or the DON-deficient ∆tri5 mutant. Extensive metabolic rearrangements mainly affect metabolites for general stress perception and signaling, reactive oxygen species (ROS) metabolism, cell wall composition, the tri-carbonic acid (TCA) cycle and γ-aminobutyric acid (GABA) shunt as well as sugar alcohols, amino acids, and storage carbohydrates. The results revealed specific, DON-related susceptibility factors. Wild-type infection resulted in an oxidative burst and the induction of plant programmed cell death, while spread of the DON-deficient mutant was blocked in a jasmonate (JA)-related defense reaction in concert with other factors. Hence, the ∆tri5 mutant is prone to defense reactions that are, in the case of a wild-type infection, not initiated.

Chitosan Hydrochloride Decreases Fusarium graminearum Growth and Virulence and Boosts Growth, Development and Systemic Acquired Resistance in Two Durum Wheat Genotypes

“…In particular, z high concentration of strobilurins inhibits the biosynthesis of ethylene (ET) [ 69 ] but improves the production of abscisic acid (ABA) [ 70 ]. It has been demonstrated that ET contributes to FHB resistance during early infection but then promotes the senescence of wheat heads that favors the fungal colonization in the dead tissues of the host [ 71 , 72 ]. On the other hand, the accumulation of ABA quickly induces the stomatal closure, which prevents the pathogen entry into the host tissues [ 73 , 74 ].…”

Unbalanced Roles of Fungal Aggressiveness and Host Cultivars in the Establishment of the Fusarium Head Blight in Bread Wheat

“…DON is the most commonly found toxin in cereals (Placinta et al, 1999). Previous works showed that DON could have a role in fungal spread beyond the initial infection (Bai et al, 2002) by facilitating the spreading of F. graminearum from spikelets into the rachis which might induce the switch from biotrophy to necrotrophy (Bönnighausen et al, 2018). DON is also known to allow the inhibition of host protein synthesis (Walter et al, 2010), and is believed to be an aggressiveness factor rather than a pathogenicity factor (Proctor et al, 1995;Pasquet et al, 2016).…”

Be flexible and adapt easily—The great role of plasticity relative to genetic variation for aggressiveness of Fusarium culmorum isolates

“…However, the association between FHB symptoms and DON accumulation at harvest might be lower when DON accumulation is normalized by fungal biomass (Miedaner, Reinbrecht, & Schilling, 2000;Voss, Bowden, Leslie, & Miedaner, 2010). DON is known to allow fungal spread beyond initial infection (Bai, Desjardins, & Plattner, 2002;Maier et al, 2006) and might even induce the switch from biotrophy to necrotrophy (Bönnighausen, Schauer, Schäfer, & Bormann, 2019). This illustrates that DON is an aggressiveness factor rather than a pathogenicity factor (Proctor, Hohn, & McCormick, 1995).…”