Victorin triggers programmed cell death and the defense response via interaction with a cell surface mediator

• Published in: Plant and cell physiology 2005-11, Vol.46 (11), p.1787-1798
• Main Authors: Tada, Y.(Kobe Univ. (Japan)), Kusaka, K, Betsuyaku, S, Shinogi, T, Sakamoto, M, Ohura, Y, Hata, S, Mori, T, Tosa, Y, Mayama, S
• Format: Article
• Language: English
• Subjects: 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide hydrochloride; 5-diaminofluorescein; APOPTOSE; APOPTOSIS; Apoptosis - physiology; Avena - cytology; Avena - physiology; AVENA SATIVA; bovine serum albumin–fluorescein derivative of victorin; Calcium - metabolism; Cell death; Cell Membrane - physiology; COCHLIOBOLUS; Cochliobolus victoriae; DAF; DCF; DEFENCE MECHANISMS; dichlorofluorescein; diphenyleneiodonium chloride; DPI; EDC; FDA; fluorescein derivative of victorin; fluorescein diacetate; Fungal Proteins - physiology; GDA; GDC; glycine decarboxylase activity; glycine decarboxylase complex; host-selective toxin; HST; Hydrogen-Ion Concentration; MECANISME DE DEFENSE; MECANISMOS DE DEFENSA; mitochondrial permeability transition; MPT; Mycotoxins - physiology; N-acetylcysteine; N-hydroxysuccinimide; NAC; NHS; PCD; Plant Leaves - cytology; Plant Leaves - physiology; Programmed cell death; reactive oxygen intermediate; ROI; SOD; superoxide dismutase; VicBSA; VicFluor; Victorin
• ISSN: 0032-0781; 1471-9053
• DOI: 10.1093/pcp/pci193

The host-selective toxin victorin is produced by Cochliobolus victoriae, the causal agent of victoria blight of oats. Victorin has been shown to bind to the P protein of the glycine decarboxylase complex (GDC) in mitochondria, and induce defense-related responses such as phytoalexin synthesis, extracellular alkalization and programmed cell death. However, evidence demonstrating that the GDC plays a critical role in the onset of cell death is still lacking, and the role of defense-like responses in the pathogenicity has yet to be elucidated. Here, cytofluorimetric analyses, using the fluorescein (VicFluor) or bovine serum albuminfluorescein derivative of victorin (VicBSA), demonstrated that victorin-induced cell death occurs before these conjugates traverse the plasma membrane. As with native victorin, VicBSA clearly elicits apoptosis-like cell death, production of phytoalexin, extracellular alkalization, and generation of nitric oxide and reactive oxygen intermediates. These results suggest that the initial recognition of victorin takes place on the cell surface, not in mitochondria, and leads to the activation of a battery of victorin-induced responses. Pharmacological studies showed that extracellular alkalization is the essential regulator for both victorin- and VicBSA-induced cellular responses. We propose a model where victorin may kill the host cell by activating an HR-like response, independent of the binding to the GDC, through ion fluxes across the plasma membrane.