Fumonisin B1-induced cell death in Arabidopsis protoplasts requires jasmonate-, ethylene-, and salicylate-dependent signaling pathways

We have established an Arabidopsis protoplast model system to study plant c ell death signaling. The fungal toxin fumonisin B1 (FB1) induces apoptosis- like programmed cell death (PCD) in wild-type protoplasts. FB1, however, on ly marginally affects the viability of protoplasts isolated from transgenic NahG plants, in which salicylic acid (SA) is metabolically degraded; from pad4-1 mutant plants, in which an SA amplification mechanism is thought to be impaired; or from jar1-1 or etr1-1 mutant plants, which are insensitive to jasmonate (JA) or ethylene (ET), respectively. FB1 susceptibility of wil d-type protoplasts decreases in the dark, as does the cellular content of p henylalanine ammonia-lyase, a light-inducible enzyme involved in SA biosynt hesis. Interestingly, however, FB1-induced PCD does not require the SA sign al transmitter NPR1, given that npr1-1 protoplasts display wild-type FB1 su sceptibility. Arabidopsis cpr1-1, cpr6-1, and acd2-2 protoplasts, in which the SA signaling pathway is constitutively activated, exhibit increased sus ceptibility to FB1, The cpr6-1 and acd2-2 mutants also constitutively expre ss the JA and ET signaling pathways, but only the acd2-2 protoplasts underg o PCD in the absence of FB1. These results demonstrate that FB1 killing of Arabidopsis is light dependent and requires SA-, JA-, and ET-mediated signa ling pathways as well as one or more unidentified factors activated by FB1 and the acd2-2 mutation.