nivalenol and Disease-Resistance

Fusarium head blight (FHB) in wheat (Triticum aestivum L.), predominantly caused by Fusarium graminearum, has been categorized into three chemotypes depending on the major mycotoxin produced. The three mycotoxins, namely, 3-acetyldeoxynivalenol (3-ADON), 15-acetyldeoxynivalenol (15-ADON) and nivalenol (NIV) also determine their aggressiveness and response to fungicides. Furthermore, prevalence of these chemotypes changes over time and dynamic changes in chemotypes population in the field have been observed. The objective of this study was to identify spike culture derived variants (SCDV) exhibiting resistance to multiple chemotypes of F. graminearum. First, the optimal volume of inoculum for point inoculation of the spikelets was determined using the susceptible AC Nanda wheat genotype. Fifteen μL of 105 macroconidia/mL was deemed optimal based on FHB disease severity assessment with four chemotypes. Following optimal inoculum volume determination, five chemotypes (Carman-NIV, Carman-705-2-3-ADON, M9-07-1-3-ADON, M1-07-2-15-ADON and China-Fg809-15-ADON) were used to point inoculate AC Nanda spikelets to confirm the mycotoxin produced and FHB severity during infection. Upon confirmation of the mycotoxins produced by the chemotypes, 55 SCDV were utilized to evaluate FHB severity and mycotoxin concentrations. Of the 55 SCDV, five (213.4, 244.1, 245.6, 250.2 and 252.3) resistant lines were identified with resistance to multiple chemotypes and are currently being utilized in a breeding program to develop wheat varieties with improved FHB resistance.

Topics: Disease Resistance; Fusarium; Mycotoxins; Plant Breeding; Trichothecenes; Triticum

Fusarium Head Blight is a disease of cereal crops that causes severe yield losses and mycotoxin contamination of grain. The main causal pathogen, Fusarium graminearum, produces the trichothecene toxins deoxynivalenol or nivalenol as virulence factors. Nivalenol-producing isolates are most prevalent in Asia but co-exist with deoxynivalenol producers in lower frequency in North America and Europe. Previous studies identified a barley UDP-glucosyltransferase, HvUGT13248, that efficiently detoxifies deoxynivalenol, and when expressed in transgenic wheat results in high levels of type II resistance against deoxynivalenol-producing F. graminearum. Here we show that HvUGT13248 is also capable of converting nivalenol into the non-toxic nivalenol-3-O-β-d-glucoside. We describe the enzymatic preparation of a nivalenol-glucoside standard and its use in development of an analytical method to detect the nivalenol-glucoside conjugate. Recombinant Escherichia coli expressing HvUGT13248 glycosylates nivalenol more efficiently than deoxynivalenol. Overexpression in yeast, Arabidopsis thaliana, and wheat leads to increased nivalenol resistance. Increased ability to convert nivalenol to nivalenol-glucoside was observed in transgenic wheat, which also exhibits type II resistance to a nivalenol-producing F. graminearum strain. Our results demonstrate the HvUGT13248 can act to detoxify deoxynivalenol and nivalenol and provide resistance to deoxynivalenol- and nivalenol-producing Fusarium.

Topics: Disease Resistance; Fusarium; Glucosyltransferases; Hordeum; Host-Pathogen Interactions; Plant Diseases; Plant Proteins; Plants, Genetically Modified; Trichothecenes; Triticum