The immune components ENHANCED DISEASE SUSCEPTIBILITY 1 and PHYTOALEXIN DEFICIENT 4 are required for cell death caused by overaccumulation of ceramides in Arabidopsis
Sphingolipid
Ceramide synthase
Phytoalexin
DOI:
10.1111/tpj.15393
Publication Date:
2021-06-28T10:42:40Z
AUTHORS (9)
ABSTRACT
Sphingolipids have key functions in plant membrane structure and signaling. Perturbations of sphingolipid metabolism often induce cell death salicylic acid (SA) accumulation; SA accumulation, turn, promotes further death. However, the underlying molecular mechanisms remain unclear. Here, we show that Arabidopsis thaliana lipase-like protein ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) its partner PHYTOALEXIN DEFICIENT 4 (PAD4) participate associated The accelerated 5 (acd5) mutants accumulate ceramides due to a defect ceramide kinase spontaneous Loss function EDS1, PAD4 or SALICYLIC ACID INDUCTION 2 (SID2) acd5 background suppressed phenotype prevented accumulation. Treatment with analogue benzothiadiazole partially restored accumulation pad4 eds1 double mutants, showing inhibitory effect pad4-1 eds1-2 mutations on acd5-conferred partly depends SA. Moreover, substantially rescued susceptibility mutant Botrytis cinerea. Consistent this, B. cinerea-induced requires EDS1. Finally, examination plants overexpressing synthase gene LAG1 HOMOLOGUE2 suggested are involved long-chain ceramide-associated Collectively, our observations reveal EDS1 mediate (especially ceramide) death, by SA-dependent SA-independent pathways.
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