treatment of wild-type seedlings with succinylacetone mimicks the sscd1 phenotypes: the treated wild-type seedlings exhibit wilted leaves and slow-growth symptoms under long-day, these symptoms are more severe under short-day. The sscd1 mutant is more sensitive to succinylacetone than the wild type under long-day
fumarylacetoacetate hydrolase hydrolyzes fumarylacetoacetate to fumarate and acetoacetate, the final step in the tyrosine degradation pathway that is essential for plant survival under short-day conditions
an Arabidopsis thaliana short-day sensitive cell death1 (sscd1) mutant displays a spontaneous cell death phenotype under short-day conditions, disruption of FAH leads to cell death, phenotype overview. The spontaneous cell death phenotype of the sscd1 mutant is completely eliminated by further knockout of the gene encoding the putative homogentisate dioxygenase, which catalyzes homogentisate into maleylacetoacetate (the antepenultimate step) in the Tyr degradation pathway. Treatment of Arabidopsis wild-type seedlings with succinylacetone, an abnormal metabolite caused by loss of FAH in the Tyr degradation pathway, mimicks the sscd1 cell death phenotype
the sscd1 mutant is hypersensitive to salt stress. The sscd1 mutant shows more accumulation of reactive oxygen species (ROS) and less up-regulation of some ROS-scavenging genes such as ASCORBATE PEROXIDASE 2 and COPPER/ZINC SUPEROXIDE DISMUTASE 1 compared with wild type under salt stress. The sscd1 mutant exhibits hypersensitivity to oxidative stress compared with wild type enzyme. Loss of fumarylacetoacetate hydrolase in sscd1 mutant leads to the accumulation of Tyr degradation intermediates, which impairs the up-regulation of some ROS-scavenging genes under salt stress, causing more accumulation of ROS, resulting in the hypersensitivity of sscd1 to salt stress
isolation and analysis of the sscd1-1 mutant. Generation of the sscd1 hgo double mutant through genetic crossing of sscd1-1 with hgo-1, an inactive homogentisate dioxygenase mutant, phenotypic analysis