Journal Article

Victorin Triggers Programmed Cell Death and the Defense Response via Interaction with a Cell Surface Mediator

Yasuomi Tada, Koh Kusaka, Shigeyuki Betsuyaku, Takeshi Shinogi, Masaru Sakamoto, Yasuko Ohura, Shingo Hata, Tomoyo Mori, Yukio Tosa and Shigeyuki Mayama

in Plant and Cell Physiology

Published on behalf of Japanese Society of Plant Physiologists

Volume 46, issue 11, pages 1787-1798
Published in print November 2005 | ISSN: 0032-0781
Published online November 2005 | e-ISSN: 1471-9053 | DOI:
Victorin Triggers Programmed Cell Death and the Defense Response via Interaction with a Cell Surface Mediator

More Like This

Show all results sharing these subjects:

  • Biochemistry
  • Molecular and Cell Biology
  • Plant Sciences and Forestry


Show Summary Details


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 albumin–fluorescein 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.

Keywords: Apoptosis; Avena sativa; Cochliobolus victoriae; Programmed cell death; Vb; Victorin; DAF, 4,5-diaminofluorescein; DCF, 2′,7′,-dichlorofluorescein; DPI, diphenyleneiodonium chloride; EDC, 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide hydrochloride; FDA, fluorescein diacetate; GDA, glycine decarboxylase activity; GDC, glycine decarboxylase complex; HST, host-selective toxin; MPT, mitochondrial permeability transition; NAC, N-acetylcysteine; NHS, N-hydroxysuccinimide; PCD, programmed cell death; ROI, reactive oxygen intermediate; SOD, superoxide dismutase; VicBSA, bovine serum albumin–fluorescein derivative of victorin; VicFluor, fluorescein derivative of victorin

Journal Article.  8301 words.  Illustrated.

Subjects: Biochemistry ; Molecular and Cell Biology ; Plant Sciences and Forestry

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.