Abstract
Phytotoxin-induced cell death is pathogen strategy for infection. To clarify the executioner of the toxin-induced cell death, we examined a fumonisin B1 (FB1)-induced cell death of Arabidopsis plants (1). FB1-induced cell death was accompanied with disruption of vacuolar membrane followed by lesion formation. The features of FB1-induced cell death were completely abolished in the Arabidopsis vacuolar processing enzyme (VPE)-null mutant, which lacks all four VPE genes. Recombinant VPE recognized a VPE substrate with Km = 30.3 μM and a caspase-1 substrate with Km = 44.2 μM, which is comparable to mammalian caspase-1. We show that VPE is a key molecule in toxin-induced cell death. Our findings suggest that a susceptible response of toxin-induced cell death is caused by the VPE-mediated vacuolar mechanism similar to a resistance response of hypersensitive cell death (2).
(1) Kuroyanagi et al., 280, 32914-32920 (2005) J. Biol. Chem.
(2) Hatsugai et al., 305, 855-858 (2004) Science
