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Fumarylacetoacetate hydrolase (FAH) catalyzes the final step in Tyr degradation pathway essential to animals but not well understood in plants. Previously, we found that mutation of  SSCD1  encoding  Arabidopsis  FAH causes cell death under short day, which uncovered an important role of Tyr degradation pathway in plants. Since phytohormones salicylic acid (SA) and jasmonate (JA) are involved in programmed cell death, in this study, we investigated whether  sscd1  cell death is related to SA and JA, and found that (1) it is accompanied by up-regulation of JA- and SA-inducible genes as well as accumulation of JA but not SA; (2) it is repressed by breakdown of JA signaling but not SA signaling; (3) the up-regulation of reactive oxygen species marker genes in  sscd1  is repressed by breakdown of JA signaling; (4) treatment of wild-type  Arabidopsis  with succinylacetone, an abnormal metabolite caused by loss of FAH, induces expression of JA-inducible genes whereas treatment with JA induces expression of some Tyr degradation genes with dependence of JA signaling. These results demonstrated that cell death resulted from loss of FAH in  Arabidopsis  is related to JA but not SA, and suggested that JA signaling positively regulates  sscd1  cell death by up-regulating Tyr degradation.

Cell death resulted from loss of fumarylacetoacetate hydrolase in Arabidopsis is related to phytohormone jasmonate but not salicylic acid