|BALDWIN, SUZETTE - University Of Idaho
|Esvelt Klos, Kathy
|MARSHALL, JULIETTE - University Of Idaho
Submitted to: PLOS ONE
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/8/2019
Publication Date: 7/12/2019
Citation: Baldwin, T.T., Arcibal, S., Bregitzer, P.P., Marshall, J., Esvelt Klos, K.L. 2019. Deletion of the benzoxazinoid detoxification gene NAT1 in Fusarium graminearum reduces deoxynivalenol in spring wheat. PLoS One. 14(7):1-14. https://doi.org/10.1371/journal.pone.0214230.
Interpretive Summary: Fusarium head blight (FHB) is a major disease of wheat caused by the fungus Fusarium graminearum. FHB causes economic loss by contaminating the wheat grains with a toxic substance called DON. Breeding highly resistant wheat varieties has been a difficult task and progress has been slow. To provide wheat breeders with a new way to develop FHB-resistant cultivars, we studied naturally occurring chemicals called benzoxazinoids. These chemicals are produced in wheat that are thought to interfere with FHB and the production of DON. We found that exposure of Fusarium graminearum to benzoxazinoids reduced DON production. Furthermore, mutant strains of Fusarium graminearum were created that lack an enzyme known to detoxify these compounds, and these strains produced less DON when inoculated on wheat. Based on our results, it may be possible to develop FHB-resistant cultivars by selecting wheats with higher levels of benzoxazinoids. Future work will seek to verify this novel approach for FHB control.
Technical Abstract: Benzoxazinoid (Bx) metabolites produced by wheat and certain other members of the Poaceae have activity against Fusarium sp. that cause cereal diseases including Fusarium head blight (FHB) on wheat and barley. Certain Bx metabolites can be detoxified by Fusarium sp. with the arylamine N-acetyltransferase NAT1. Investigation of this pathway may reveal strategies for increasing FHB resistance, such as selection for higher levels of Bx metabolites within existing germplasm and/or engineering fungal susceptibility via host induced silencing of NAT1. We assessed the reactions of fifteen wheat cultivars or breeding lines adapted to the Northwestern United States to infection with F. graminearum 'nat1 mutants that should be sensitive to Bx metabolites. Significant differences were noted in disease severity and DON among the cultivars 21 d after inoculation with either mutant or wildtype (PH1) strains. Mutant vs. wildtype strains did not result in significant variation for infection severity (as measured by % infected florets), but inoculation with 'nat1 mutants vs. wildtype resulted in significantly lower DON concentrations in mature kernels (p < 0.0001). Of the cultivars tested, HRS3419 was the most resistant cultivar to PH1 (severity = 62%, DON = 45 ppm) and 'nat1 mutants (severity = 61%, DON = 30 ppm). The cultivar most susceptible to infection was Kelse with PH1 (severity = 100%, DON = 292 ppm) and 'nat1 mutants (severity = 100%, DON = 158 ppm). We hypothesized that sub-lethal Bx metabolite levels may suppress DON production in F. graminearum 'nat1 mutants. In vitro assays of Bx metabolites BOA, MBOA, and DIMBOA at 30 µM did not affect growth, but did reduce DON production by 'nat1 and PH1. Although the levels of Bx metabolites are likely too low in the wheat cultivars we tested to suppress FHB, higher levels of Bx metabolites may contribute towards reductions in DON and FHB.