Fumarylacetoacetate Hydrolase Regulates Seed Dormancy and Germination Through the Gibberellin Pathway in Arabidopsis

Tyrosine (Tyr) degradation is a crucial pathway in animals. However, its role in plants remains to be examined. Fumarylacetoacetate hydrolase (FAH) is the final enzyme involved in Tyr degradation. Studies of a mutant of the <i>SHORT-DAY SENSITIVE CELL DEATH 1</i> (<i>SSCD1</i>) gene encoding FAH in Arabidopsis have shown that blockage of this pathway results in the accumulation of Tyr metabolites, thereby inducing cell death under short-day conditions. Seed dormancy is a critical trait which is regulated by endogenous and environmental cues, among which abscisic acid (ABA) and gibberellin (GA) are the primary effectors. ABA induces seed dormancy, whereas GA releases seed dormancy. In this study, <i>sscd1</i> seeds displayed deep dormancy and hypersensitivity to the GA biosynthesis inhibitor paclobutrazol, but not to ABA during germination. However, exogenous GA₃ could not completely recover dormancy or germination of <i>sscd1</i> seeds. Moreover, GA₃ level was reduced, which was consistent with the decreased expression of <i>GA3-oxidase 1</i> in imbibed <i>sscd1</i> seeds. Furthermore, <i>SSCD1</i> acted upstream of <i>RGA-LIKE 2</i>. Eliminating the accumulation of Tyr metabolites by inhibiting homogentisate dioxygenase, an enzyme upstream of FAH, completely rescued the phenotype of <i>sscd1</i> seeds. Additionally, germination of <i>sscd1</i> seeds was hypersensitive to FAH deficiency-induced accumulation of succinylacetone, which is a Tyr metabolite. These findings suggest that FAH deficiency in <i>sscd1</i> causes accumulation of Tyr metabolites, thereby disrupting GA biosynthesis and signaling. This resulted in deep dormancy and hypersensitivity to paclobutrazol during germination and highlights the important role of the Tyr degradation pathway in GA-mediated seed dormancy and germination.