Introduction
Seed dormancy and germination
The emergence of seed-bearing plants represents a crucial time-point in their adaptation from water to land. The reasons for the success of seed plants in the colonization of land lie not only in the diverse plasticity and anatomy of seeds that enclose an embryo, but also in the different strategies that allow seeds to overcome environmental challenges. The most prominent strategy is the maintenance of a quiescent state between the period of seed maturation and the resumption of growth that occurs as a germination under favorable conditions. The simplest way to impose dormancy on a seed is a biophysical barrier around it that prevents the exchange of water and gases. However, in most cases, a physiological dormancy is imposed by the intrinsic seed tissues -- the embryo and endosperm -- that prevent germination until appropriate triggers for germination are present. Physical and physiological dormancy are not mutually exclusive as the seed coat can act biomechanically, thereby contributing to the physiological dormancy. For example, the seed coat in Arabidopsis can control the timing of germination by inhibiting the leaching out of embryo growth inhibitors such as ABA. Since the discovery of 'dormin' (now referred to as ABA) as the factor behind dormancy and of GA as a promoter of germination, the ratio of ABA/GA has been identified as an important factor in determining whether a seed sprouts or not. Genetic mutants of Arabidopsis that are impaired either in the synthesis of ABA or in downstream signals generated by it produce non-dominant seeds, which germinate even in the absence of favorable conditions. It has been shown that other hormones such as ET, AUX and JA can also play a role in breaking dormancy and simulating germination. Freshly harvested Arabidopsis seeds usually have a physiological dormancy that can be weakened by cold stratification in the fully imbibed state or by after-ripening, which is a period (usually several months) of dry storage at room temperature. There is a good degree of understanding of the hormonal mechanisms associated with dormancy and germination in greater detail. Previous studies have focused on the ecological, physiological, or modeled aspects of the mechanisms that generate variability or bet-hedging in plants. In this review, we focus on the molecular and cellular mechanisms that generate variability within the processes leading to dormancy and subsequent germination among individual and genetically identical seeds. Here, we focus on the intrinsic factors rather than environmental ones that affect variability among primary dormant seeds and on recent developments in the model plant Arabidopsis, where considerable advances are being made at the level of single seeds and cells.
Authors: Sharma and Majee
Introduction Seed dormancy and germination The emergence of seed-bearing plants represents a crucial time-point in their adaptation from water to land. The reasons for the success of seed plants in the colonization of land lie not only in the diverse plasticity and anatomy of seeds that enclose an embryo, but also in the different strategies that allow seeds to overcome environmental challenges. The most prominent strategy is the maintenance of a quiescent state between the period of seed maturation and the resumption of growth that occurs as a germination under favorable conditions. The simplest way to impose dormancy on a seed is a biophysical barrier around it that prevents the exchange of water and gases. However, in most cases, a physiological dormancy is imposed by the intrinsic seed tissues -- the embryo and endosperm -- that prevent germination until appropriate triggers for germination are present. Physical and physiological dormancy are not mutually exclusive as the seed coat can act biomechanically, thereby contributing to the physiological dormancy. For example, the seed coat in Arabidopsis can control the timing of germination by inhibiting the leaching out of embryo growth inhibitors such as ABA. Since the discovery of 'dormin' (now referred to as ABA) as the factor behind dormancy and of GA as a promoter of germination, the ratio of ABA/GA has been identified as an important factor in determining whether a seed sprouts or not. Genetic mutants of Arabidopsis that are impaired either in the synthesis of ABA or in downstream signals generated by it produce non-dominant seeds, which germinate even in the absence of favorable conditions. It has been shown that other hormones such as ET, AUX and JA can also play a role in breaking dormancy and simulating germination. Freshly harvested Arabidopsis seeds usually have a physiological dormancy that can be weakened by cold stratification in the fully imbibed state or by after-ripening, which is a period (usually several months) of dry storage at room temperature. There is a good degree of understanding of the hormonal mechanisms associated with dormancy and germination in greater detail. Previous studies have focused on the ecological, physiological, or modeled aspects of the mechanisms that generate variability or bet-hedging in plants. In this review, we focus on the molecular and cellular mechanisms that generate variability within the processes leading to dormancy and subsequent germination among individual and genetically identical seeds. Here, we focus on the intrinsic factors rather than environmental ones that affect variability among primary dormant seeds and on recent developments in the model plant Arabidopsis, where considerable advances are being made at the level of single seeds and cells.