Abstract
Pyrenophora tritici-repentis (Ptr), a necrotrophic fungus and the causal agent of tan spot of wheat, produces one or a combination of host-selective toxins (HSTs) necessary for disease development. The two most studied toxins produced by Ptr, Ptr ToxA (ToxA) and Ptr ToxB (ToxB), are proteins that cause necrotic or chlorotic symptoms respectively. Investigation of host responses induced by HSTs provides better insight into the nature of the host susceptibility. Microarray analysis of ToxA has provided evidence that it can elicit responses similar to those associated with defense. In order to evaluate whether there are consistent host responses associated with susceptibility, a similar analysis of ToxB-induced changes in the same sensitive cultivar was conducted. Comparative analysis of ToxA- and ToxB-induced transcriptional changes showed that similar groups of genes encoding WRKY transcription factors, RLKs, PRs, components of the phenylpropanoid and jasmonic acid pathways are activated. ROS accumulation and photosystem dysfunction proved to be common mechanism-of-action for these toxins. Despite similarities in defense responses, transcriptional and biochemical responses as well as symptom development occur more rapidly for ToxA compared to ToxB, which could be explained by differences in perception as well as by differences in activation of a specific process, for example, ethylene biosynthesis in ToxA treatment. Results of this study suggest that perception of HSTs will result in activation of defense responses as part of a susceptible interaction and further supports the hypothesis that necrotrophic fungi exploit defense responses in order to induce cell death.
Highlights
Plant pathogen interactions that exhibit classical gene-for-gene characteristics have provided a fundamental model for the molecular genetic evaluation of disease development and plant defense
In order to determine if ToxA and ToxB induce similar responses and to begin to understand the differences between the mechanisms that induce necrosis vs. chlorosis, we investigated the transcriptome changes that occur in Katepwa as a consequence of ToxB treatment and compared these to our previously published transcriptome analysis of ToxA treatment of the same cultivar
To explore and characterize the underlying mechanisms of susceptibility to a necrotrophic pathogen, we investigated plant responses to the hostselective toxins (HSTs) ToxB, and compared them to the responses evoked in leaves treated with the HST ToxA [44]
Summary
Plant pathogen interactions that exhibit classical gene-for-gene characteristics have provided a fundamental model for the molecular genetic evaluation of disease development and plant defense. Host resistance (incompatibility) in classical gene-for-gene interactions requires the recognition of the product of a pathogen avirulence (Avr) gene by a complementary plant resistance (R) gene. The genetic tractability of this model allowed for a better understanding of the role that pathogen effectors’ play in conferring avirulence and their contribution to virulence in the absence of Avr/R recognition. Continuous efforts have been directed towards determining the mechanisms by which pathogen effectors condition host susceptibility. The identification and characterization of these types of effectors (pathogenicity factors) is integral for understanding the physiological nature of plant disease susceptibility. Cases where a single gene/locus conditions sensitivity to a given HST and susceptibility rather than resistance to the pathogen represent an ‘‘inverse’’ of the classical gene-for-gene interaction [1,2]
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