Sucrose rescues seedling establishment but not germination of Arabidopsis mutants disrupted in peroxisomal fatty acid catabolism

Abstract

Summary: The Arabidopsis acyl‐CoA oxidase (ACX) family comprises isozymes with distinct fatty acid chain‐length specificities that together catalyse the first step of peroxisomal fatty acid β‐oxidation. We have isolated and characterized T‐DNA insertion mutants in the medium to long‐chain (ACX1) and long‐chain (ACX2) acyl‐CoA oxidases, and show that the corresponding endogenous activities are decreased in the mutants. Lipid catabolism during germination and early post‐germinative growth was unaltered in the acx1‐1 mutant, but slightly delayed in the acx2‐1 mutant, with 3‐day‐old acx2‐1 seedlings accumulating long‐chain acyl‐CoAs. In acx1‐1 and acx2‐1, seedling growth and establishment in the absence of an exogenous supply of sucrose was unaffected. Seedlings of the double mutant acx1‐1 acx2‐1 were unable to catabolize seed storage lipid, and accumulated long‐chain acyl‐CoAs. The acx1‐1 acx2‐1 seedlings were also unable to establish photosynthetic competency in the absence of an exogenous carbon supply, a phenotype that is shared with a number of other Arabidopsis mutants disrupted in storage lipid breakdown. Germination frequency of the double mutant was significantly reduced compared with wild‐type seeds. This was unaffected by the addition of exogenous sucrose, but was improved by dormancy‐breaking treatments such as cold stratification and after‐ripening. We show that the acx1‐1, acx2‐1 and acx1‐2 acx2‐1 double mutants and the ketoacyl‐CoA thiolase‐2 (kat2) mutant exhibit a sucrose‐independent germination phenotype comparable with that reported for comatose (cts‐2), a mutant in a peroxisomal ABC transporter which exhibits enhanced dormancy. This demonstrates an additional role beyond that of carbon provision for the β‐oxidation pathway during germination or in dormant seeds.