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α‐Tomatine, the major saponin in tomato, induces programmed cell death mediated by reactive oxygen species in the fungal pathogen Fusarium oxysporum
Author(s) -
Ito Shin-ichi,
Ihara Takashi,
Tamura Hideyuki,
Tanaka Shuhei,
Ikeda Tsuyoshi,
Kajihara Hiroshi,
Dissanayake Chandrika,
Abdel-Motaal Fatma F.,
El-Sayed Magdi A.
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.06.010
Subject(s) - fusarium oxysporum , programmed cell death , biology , reactive oxygen species , cycloheximide , depolarization , biochemistry , microbiology and biotechnology , saponin , mitochondrion , apoptosis , botany , protein biosynthesis , biophysics , medicine , alternative medicine , pathology
The tomato saponin α‐tomatine has been proposed to kill sensitive cells by binding to cell membranes followed by leakage of cell components. However, details of the modes of action of the compound on fungal cells are poorly understood. In the present study, mechanisms involved in α‐tomatine‐induced cell death of fungi were examined using a filamentous pathogenic fungus Fusarium oxysporum . α‐Tomatine‐induced cell death of F. oxysporum (TICDF) occurred only under aerobic conditions and was blocked by the mitochondrial F 0 F 1 ‐ATPase inhibitor oligomycin, the caspase inhibitor D‐VAD‐fmk, and protein synthesis inhibitor cycloheximide. Fungal cells exposed to α‐tomatine showed TUNEL‐positive nuclei, depolarization of transmembrane potential of mitochondria, and reactive oxygen species (ROS) accumulation. These results suggest that TICDF occurs through a programmed cell death process in which mitochondria play a pivotal role. Pharmacological studies using inhibitors suggest that α‐tomatine activates phosphotyrosine kinase and monomeric G‐protein signaling pathways leading to Ca 2+ elevation and ROS burst in F. oxysporum cells.