Genetic differences in seed longevity of various Arabidopsis mutants

Seeds gradually lose their viability during dry storage. The damage that occurs at the biochemical level can alter the seed physiological status and is affected by the storage conditions of the seeds. Although these environmental conditions controlling loss of viability have been investigated frequently, little information is available on the genetics of seed longevity. Using Arabidopsis mutants in defined developmental or biochemical pathways such as those affected in seed coat composition, seed dormancy, hormone function and control of oxidative stress, we tried to gain insight into the genes and mechanisms controlling viability of stored seeds. Mutations like abscisic acid insensitive3 (abi3) as well as abscisic acid deficient1 (aba1) show reduced longevity, which may be partially related to the seed dormancy phenotype of these mutants. Mutants with seed coat alterations, especially aberrant tests shape (ats), showed a stronger reduction in germination percentage after storage, indicating the importance of a 'functional' seed coat for seed longevity. A specific emphasis was placed on mutants affected in dealing with Reactive Oxygen Species (ROS). Because several pathways are involved in protection against ROS and because gene redundancy is a common feature in Arabidopsis, 'double' mutants were generated. These 'double' mutants and the corresponding single mutants were subjected to a controlled deterioration test (CDT) and a germination assay on hydrogen peroxide (H2O2) after prolonged storage at two relative humidities. CDT and germination on H2O2 affected all genotypes, although it appears that other effects like genetic background are more important than the deficiencies in the ROS scavenging pathway. Explanations for this limited effect of mutations affecting ROS scavenging are discussed.