Involvement of ethylene in seed physiology

The seed, the organ by which higher plants perpetuate themselves, is programmed to survive after being dispersed from the mother plant until establishing a photosynthetically competent seedling. Seed dormancy, conceived as the temporary failure of an intact viable seed to complete germination under favourable conditions, is developed during the last period of embryogenesis and prevents germination during periods unfavourable to seedling growth and development. Therefore, seed dormancy is an adaptive mechanism to ensure plant survival. The breaking of dormancy involves physiological and molecular changes that affect the subsequent germination response. Seed dormancy is a complex trait under the control of a large number of genes. Genetic and physiological evidence strongly indicate that abscisic acid (ABA) is key in establishing and maintaining seed dormancy and that gibberellins (GAs) are important for germination and for counteracting ABA effects in seed dormancy. In general, ABA delays or prevents seed germination and determines the depth of dormancy during development, whereas GAs breaks dormancy and promotes germination upon imbibition in some mature seeds. Since many species produce ethylene (ET) during last period of embryogenesis and germination, and some factors that break dormancy also stimulate its production, it has been proposed that ET production may contribute to the breaking of dormancy in some species. Biochemical and genetic approaches continue to shed light on aspects of the mechanism of dormancy and germination by identifying ET-mutants and genes that control these processes. This review updates and discusses the effects of ET in relation to the process of acquisition and loss of seed dormancy.