*2.2.1 Seed maturity*

Seed maturation is the second phase of seed development after embryogenesis during which food reserves accumulate, while dormancy and desiccation tolerance develops [31]. In angiosperms, there is increasing evidence that maternal environmental effects affect both germination percentage and germination phenology [32]. Environmental factors that affect the mother plant, such as photoperiod and temperature, during seed maturation have also been found to influence seed germination of many species [33]. These factors may also influence the size of the seeds, which in turn may influence germination timing and success [34], and within species, seed mass is often associated with probability or time of germination [35]. Identifying the

environmental mechanisms involved in the transmission of maternal environmental effects through the seeds is important to understand their ecological function and adaptive value [32].

### *2.2.2 Plant growth regulator (PGR)*

ABA, GA, ethylene, brassinosteroids, auxins, and cytokinins have a tremendous effect on plant development, even at low concentrations among all PGR [36]. Even though PGR like cytokinin, auxins ethylene and brassinosteroids can either promote germination alone or in association with ABA, most literature on hormonal regulation of seed germination suggests that induction and release of dormancy is controlled by two main plant growth regulators notably ABA and GA. However, the influence of these two hormones is mainly at the variation in their ratio than their absolute content. Thus, dormancy induction would depend on ABA and GA metabolism during the process. Any metabolic processes that can change the concentration of the active forms of IBA and GA within the seed like synthesis, degradation, activation or deactivation will either induce or break dormancy. Thus any metabolic process that synthesizes or activates IBA induces dormancy because such processes turn to degrade or deactivate GA, given that these two hormones are antagonistic. Increase of seed to ABA sensitivity, and decrease of GA sensitivity induce dormancy and the opposite events will lead to dormancy alleviation and germination [37].

#### *2.2.2.1 Abscissic acid*

ABA is a sesquiterpene hormone that plays an integral part in mediating the adaptation of the plant to biotic and abiotic environmental stresses, regulation of seed development and germination. During seed development, ABA concentration increases intensely during embryogenesis to promote accumulation of reserves, prevent precocious germination, promote embryo tolerance during seed desiccation phase, and induction of dormancy at dispersal [38]. ABA is a main plant growth regulator of dormancy induction and maintenance [1]. Insensitivity to ABA during seed development results to precocious seed germination. This has been observed in maize, tomato, and Arabidopsis mutants deficient in ABA content [39, 40].

In spite of the fact that the relationship between ABA content and its physiological function in seed dormancy and germination is still to be made clear, more light has been shed on mechanisms surrounding ABA-mediated seed germination inhibition. It is the case in *Brassica napus*, where it was suggested that one of the probable contribution of ABA to inhibiting germination is to prevent loosening of the embryo cell wall which impedes water uptake [41]. In addition, ABA has also been found to specifically inhibit endosperm rupture instead of testa rupture. The effect of ABA on seed dormancy can be efficiently alleviated by chilling 'stratification treatment' so that endogenous ABA content drops precipitously with a concurrent increase in germination rate [42]. This inhibitory effect can be partially counteracted by the antagonistic action of GA [43].
