Regulation of seed dormancy by abscisic acid and DELAY OF Germination 1

Dekkers, S.J.W.; Bentsink, L.


Physiological dormancy has been described as a physiological inhibiting mechanism that prevents radicle emergence. It can be caused by the embryo (embryo dormancy) as well as by the structures that cover the embryo. One of its functions is to time plant growth and reproduction to the most optimal season and therefore, in nature, dormancy is an important adaptive trait that is under selective pressure. Dormancy is a complex trait that is affected by many loci, as well as by an intricate web of plant hormone interactions. Moreover, it is strongly affected by a multitude of environmental factors. Its induction, maintenance, cycling and loss come down to the central paradigm, which is the balance between two key hormonal regulators, i.e. the plant hormone abscisic acid (ABA), which is required for dormancy induction, and gibberellins (GA), which are required for germination. In this review we will summarize recent developments in dormancy research (mainly) in the model plant Arabidopsis thaliana, focusing on two key players for dormancy induction, i.e. the plant hormone ABA and the DELAY OF GERMINATION 1 (DOG1) gene. We will address the role of ABA and DOG1 in relation to various aspects of seed dormancy, i.e. induction during seed maturation, loss during dry seed afterripening, the rehydrated state (including dormancy cycling) and the switch to germination.