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

## TL;DR

This study shows that a specific enzyme in plants affects seed dormancy and germination by influencing a key hormone pathway.

## Contribution

The study reveals a novel role of fumarylacetoacetate hydrolase in regulating gibberellin signaling during seed dormancy and germination in Arabidopsis.

## Key findings

- FAH deficiency in sscd1 seeds leads to accumulation of Tyr metabolites and deep dormancy.
- GA3 levels and GA3-oxidase 1 expression are reduced in sscd1 seeds.
- Inhibiting Tyr metabolite accumulation rescues sscd1 seed dormancy and germination.

## Abstract

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 SHORT-DAY SENSITIVE CELL DEATH 1 (SSCD1) 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, sscd1 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 sscd1 seeds. Moreover, GA3 level was reduced, which was consistent with the decreased expression of GA3-oxidase 1 in imbibed sscd1 seeds. Furthermore, SSCD1 acted upstream of RGA-LIKE 2. Eliminating the accumulation of Tyr metabolites by inhibiting homogentisate dioxygenase, an enzyme upstream of FAH, completely rescued the phenotype of sscd1 seeds. Additionally, germination of sscd1 seeds was hypersensitive to FAH deficiency-induced accumulation of succinylacetone, which is a Tyr metabolite. These findings suggest that FAH deficiency in sscd1 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.