Research articleSphingosine kinase AtSPHK1 functions in fumonisin B1-triggered cell death in Arabidopsis

- The mycotoxin FB1 can trigger plant cell death that adversely affects plant development and crop production.
- The key regulatory components involved in FB1 action in plants remain to be identified at the molecular level.
- Sphingosine kinase SPHK1 potentiates FB1 killing of plants by enhancing SA action and ROS accumulation.
- Suppression of SPHK1 increases plant resistance to FB1 stress through promoting JA production.
- SPHK1 plays a role in modulating FB1-triggered cell death by accessing the SA and JA signalling pathways in Arabidopsis.

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.