Abstract
This review aims to summarize our major findings on the host physiology affected by wheat blast caused by Pyricularia oryzae and disease management with emphasis on mineral nutrition and fungicides. Infected plants show reduced values of the leaf gas exchange parameters net carbon assimilation rate, stomatal conductance, and transpiration rate and greater values of internal CO2 concentration. Indeed, the photosynthetic machinery is damaged as suggested by reductions in the maximum quantum quenching, photochemical quenching coefficient and electron transport rate. A decrease in the concentration of photosynthetic pigments also occurs. Wheat resistance to blast is intrinsically associated with an increase in the production of reactive oxygen species (ROS), which favors host defense mechanisms against P. oryzae infection. In fact, a more efficient antioxidative system that removes the excess of ROS generated during the infection process of P. oryzae prevents the cellular damage caused by the fungus. As to mineral nutrition, plants supplied with high silicon and low magnesium rate exhibited reduced concentrations of ROS and a more efficient antioxidant system, thus preserving the photosynthetic performance. The expression levels of the defense-related genes pathogenesis-related 1, chitinase, peroxidase and phenylalanine ammonia-lyase were from 2- to 3-fold higher in silicon-amended plants, which showed leaf and rachis lesser colonized by the fungus. Wheat cultivars able to activate defense mechanisms against P. oryzae infection, thus possessing a more efficient antioxidant system, are recommended. However, fungicides applied during flowering time, in addition to host resistance, are necessary to achieve better control of head blast and reduce yield loss under conditions favorable for the disease.
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Section Editor: Emerson M. Del Ponte
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Rodrigues, F.Á., Rios, J.A., Debona, D. et al. Pyricularia oryzae-wheat interaction: physiological changes and disease management using mineral nutrition and fungicides. Trop. plant pathol. 42, 223–229 (2017). https://doi.org/10.1007/s40858-017-0130-z
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DOI: https://doi.org/10.1007/s40858-017-0130-z