Plant responses induced by Ptr ToxA and Ptr ToxB, host-selective toxins produced by Pyrenophora tritici-repentis. Public Deposited


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  • Pyrenophora tritici-repentis (Ptr) is the causal agent of the disease tan spot of wheat, which can be responsible for the destruction of up to 50% of a wheat crop harvest. Tan spot disease results in chlorotic and/or necrotic lesions triggered by the pathogen’s production of one or several host-selective toxins (HSTs). HSTs are diverse metabolites that dictate disease development only on susceptible hosts; therefore, they function as determinants of pathogenicity or virulence. Ptr produces two proteinaceous HSTs, Ptr ToxA (ToxA) and Ptr ToxB (ToxB). In toxin sensitive wheat cultivars ToxA and ToxB induce necrosis and chlorosis, respectively. The current model of ToxA mode-of-action involves binding of ToxA to an uncharacterized receptor on sensitive mesophyll cells that mediates ToxA internalization, allowing the toxin to localize to the chloroplast. This leads to an increase in the levels of reactive oxygen species (ROS) in the chloroplast. Because 2 less is known about ToxB mode-of-action, we initiated studies to compare and contrast plant responses to both toxins. Initially, we sought to determine whether ROS accumulation occurs in response to ToxB. Additionally, we measured the production of phenolic compounds and phenylalanine ammonia lyase (PAL) activity, important components of the defense-related phenylpropanoid pathway. Our results indicate that: 1) ROS accumulation occurs in the chloroplast after ToxB treatment of the toxin-sensitive cultivar; 2) antioxidant N-acetylecysteine decreases symptom development induced by ToxB, 3) both toxins induced accumulation of soluble phenolic compounds in the toxin-sensitive cultivar, and 4) PAL activity is elevated in ToxA and ToxB-treated sensitive leaves compared to water-treated controls. These data suggest that ToxA and ToxB induce similar responses in the sensitive wheat cultivar.
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