Host-selective toxins of Pyrenophora tritici-repentis induce common responses associated with host susceptibility.
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.
Department of Botany and Plant Pathology and Center for Genome Research and Biocomputing, Oregon State University, Corvallis, Oregon, United States of America.
Iovanna
I
Pandelova
Melania
M
Figueroa
Larry J
LJ
Wilhelm
Viola A
VA
Manning
Aakash N
AN
Mankaney
Todd C
TC
Mockler
Lynda M
LM
Ciuffetti
D001203:Ascomycota / Q000472:pathogenicity*; D016923:Cell Death / Q000187:drug effects; D020869:Gene Expression Profiling; D018506:Gene Expression Regulation, Plant / Q000187:drug effects; D020022:Genetic Predisposition to Disease; D054884:Host-Pathogen Interactions / Q000235:genetics; D053858:Metabolic Networks and Pathways / Q000187:drug effects; D005810:Multigene Family / Q000187:drug effects; D009183:Mycotoxins / Q000494:pharmacology*; D018384:Oxidative Stress / Q000235:genetics; D010788:Photosynthesis / Q000187:drug effects; D010935:Plant Diseases / Q000235:genetics* / Q000382:microbiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D014908:Triticum / Q000235:genetics* / Q000382:microbiology*
D009183:Mycotoxins; D017382:Reactive Oxygen Species