fumonisin-b1 and jasmonic-acid

The fungal toxin Fumonisin B1 (FB1) is a strong inducer to trigger plant hypersensitive responses (HR) along with increased long chain bases (LCB) and long chain base phosphates (LCBP) contents, though the regulatory mechanism of FB1 action and how the LCB/LCBP signalling cassette functions during the process is still not fully understood. Here, we report sphingosine kinase 1 (SPHK1) as a key factor in FB1-induced HR by modulating the salicylic acid (SA) pathway and reactive oxygen species (ROS) accumulation in Arabidopsis thaliana. Overexpression of SPHK1 increases the FB1-induced accumulations of ROS and SA. The double mutant that simultaneously overexpresses SPHK1 and suppresses the SPPASE or DPL1, two enzymes are mainly responsible for Phyto-sphingosine-1-phosphate (Phyto-S1P) removal, showed enhanced susceptibility to FB1 killing and FB1-induced SA activation than the plants overexpress SPHK1 alone. Exogenous sphingosine-1-phosphate (S1P) can modulate the transcription of the SA-responsive marker gene PR1 in a concentration-dependent biphasic manner. Suppression of SPHK1 decreases SA production whereas promotes jasmonic acid (JA) biosynthesis in response to FB1 applications. Our findings indicate a role of SPHK1 in modulating FB1-triggered cell death via SA and JA pathway interactions.

Topics: Arabidopsis; Arabidopsis Proteins; Cell Death; Cyclopentanes; Fumonisins; Oxylipins; Phosphotransferases (Alcohol Group Acceptor); Salicylic Acid

The mycotoxin fumonisin B1 (FB1) is a strong inducer of programmed cell death (PCD) in plants, but its underlying mechanism remains unclear. Here, we describe two ubiquitin ligases, RING DOMAIN LIGASE3 (RGLG3) and RGLG4, which control FB1-triggered PCD by modulating the jasmonate (JA) signalling pathway in Arabidopsis thaliana. RGLG3 and RGLG4 transcription was sensitive to FB1. Arabidopsis FB1 sensitivity was suppressed by loss of function of RGLG3 and RGLG4 and was increased by their overexpression. Thus RGLG3 and RGLG4 have coordinated and positive roles in FB1-elicited PCD. Mutated JA perception by coi1 disrupted the RGLG3- and RGLG4-related response to FB1 and interfered with their roles in cell death. Although FB1 induced JA-responsive defence genes, it repressed growth-related, as well as JA biosynthesis-related, genes. Consistently, FB1 application reduced JA content in wild-type plants. Furthermore, exogenously applied salicylic acid additively suppressed JA signalling with FB1 treatment, suggesting that FB1-induced salicylic acid inhibits the JA pathway during this process. All of these effects were attenuated in rglg3 rglg4 plants. Altogether, these data suggest that the JA pathway is hijacked by the toxin FB1 to elicit PCD, which is coordinated by Arabidopsis RGLG3 and RGLG4.

Topics: Apoptosis; Arabidopsis; Arabidopsis Proteins; Cell Nucleus; Cyclopentanes; Cytoplasm; Fumonisins; Gene Expression Regulation, Plant; Ligases; Oxylipins; RING Finger Domains; Salicylic Acid; Signal Transduction

Programmed cell death (PCD) is a crucial process for plant innate immunity and development. In plant innate immunity, PCD is believed to prevent the spread of pathogens from the infection site. Although proper control of PCD is important for plant fitness, we have limited understanding of the molecular mechanisms regulating plant PCD. Plant innate immunity triggered by recognition of effectors (effector-triggered immunity, ETI) is often associated with PCD. However pattern-triggered immunity (PTI), which is triggered by recognition of elicitors called microbe-associated molecular patterns (MAMPs), is not. Therefore we hypothesized that PTI might suppress PCD. Here we report that PCD triggered by the mycotoxin fumonisin B1 (FB1) can be suppressed by PTI in Arabidopsis. FB1-triggered cell death was suppressed by treatment with the MAMPs flg22 (a part of bacterial flagellin) or elf18 (a part of the bacterial elongation factor EF-Tu) but not chitin (a component of fungal cell walls). Although plant hormone signaling is associated with PCD and PTI, both FB1-triggered cell death and suppression of cell death by flg22 treatment were still observed in mutants deficient in jasmonic acid (JA), ethylene (ET) and salicylic acid (SA) signaling. The MAP kinases MPK3 and MPK6 are transiently activated and inactivated within one hour during PTI. We found that FB1 activated MPK3 and MPK6 about 36-48 hours after treatment. Interestingly, this late activation was attenuated by flg22 treatment. These results suggest that PTI suppression of FB1-triggered cell death may involve suppression of MPK3/MPK6 signaling but does not require JA/ET/SA signaling.

Topics: Arabidopsis; Arabidopsis Proteins; Bacterial Proteins; Cell Death; Chitin; Cyclopentanes; Ethylenes; Flagellin; Fumonisins; Gene Expression Regulation, Plant; Mitogen-Activated Protein Kinase Kinases; Mitogen-Activated Protein Kinases; Mycotoxins; Oxylipins; Peptide Elongation Factor Tu; Peptide Fragments; Plant Growth Regulators; Plant Immunity; Salicylic Acid; Signal Transduction

We have established an Arabidopsis protoplast model system to study plant cell death signaling. The fungal toxin fumonisin B1 (FB1) induces apoptosis-like programmed cell death (PCD) in wild-type protoplasts. FB1, however, only 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 wild-type protoplasts decreases in the dark, as does the cellular content of phenylalanine ammonia-lyase, a light-inducible enzyme involved in SA biosynthesis. Interestingly, however, FB1-induced PCD does not require the SA signal transmitter NPR1, given that npr1-1 protoplasts display wild-type FB1 susceptibility. Arabidopsis cpr1-1, cpr6-1, and acd2-2 protoplasts, in which the SA signaling pathway is constitutively activated, exhibit increased susceptibility to FB1. The cpr6-1 and acd2-2 mutants also constitutively express the JA and ET signaling pathways, but only the acd2-2 protoplasts undergo PCD in the absence of FB1. These results demonstrate that FB1 killing of Arabidopsis is light dependent and requires SA-, JA-, and ET-mediated signaling pathways as well as one or more unidentified factors activated by FB1 and the acd2-2 mutation.

Topics: Arabidopsis; Carboxylic Acids; Cell Death; Cyclopentanes; Ethylenes; Fumonisins; Oxylipins; Plant Growth Regulators; Protoplasts; Salicylates; Signal Transduction