Pathogen Triggered Plant Volatiles Induce Systemic Susceptibility in Neighboring Plants
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This project elucidates the effect of volatile organic compounds (VOCs) emitted by maize infected with fungal pathogens on disease progression in neighboring plants. To protect themselves from herbivory by insects, plants initiate a multifaceted defense response. In contrast to direct defense, characterized by the production of toxic metabolites, indirect defense relies on volatile emissions to attract predators of the insect herbivores as well as warning neighboring plants to prepare for insect attack. This biochemically diverse bouquet of volatiles produced in response to insect feeding is known as herbivore-induced plant volatiles (HIPVs). One subgroup of HIPVs is Green Leaf Volatiles (GLVs), which govern plant-plant and plant-insect communication, as well as endogenous defensive signaling. Despite the strategic role of GLVs in insect defense, their function during microbial interactions has been widely overlooked. Herbivory induced GLVs prime neighboring plants against impending insect attack by enabling them to produce greater levels of jasmonic acid (JA) when challenged with an infestation. This priming phenomenon is called induced systemic resistance (ISR). Despite the strategic role of GLVs in insect defense, their function in direct and indirect defenses against pathogens has been largely overlooked. Unexpectedly, pathogen-induced plant volatiles (PIPVs) induce systemic susceptibility (ISS) in neighboring plants, rather than ISR, as the receiver plants exposed to PIPVs from infected plants became significantly more susceptible to C. graminicola and Cochliobolus heterostrophus. Susceptibility in neighboring plants is caused by the release of GLVs from infected plants that induces the positive regulation and biosynthesis of JA in neighboring plants. JA has been shown to promote susceptibility to C. graminicola. LOX2, LOX5, LOX12 and OPR2 are PIPV and GLV inducible genes that are involved in JA regulation and biosynthesis in maize and are vital to the induction of ISS in PIPV exposed receiver plants. In summary, this research illustrates a novel model for explaining how pathogen infections may spread under epidemic-prone conditions in the field. In this model, volatile emissions from infected plants predispose neighboring plants to become a more suitable host for an imminent infection.
