Molecular Mechanisms Underlying Abscisic Acid/Gibberellin Balance in the Control of Seed Dormancy and Germination in Cereals

Abstract

Seed dormancy is an adaptive trait that does not allow the germination of an intact viable seed under favorable environmental conditions. Non-dormant seeds or seeds with low level of dormancy can germinate readily under optimal environmental conditions, and such a trait leads to preharvest sprouting, germination of seeds on the mother plant prior to harvest, which significantly reduces the yield and quality of cereal crops. High level of dormancy, on the other hand, may lead to non-uniform germination and seedling establishment. Therefore, intermediate dormancy is considered to be a desirable trait as it prevents the problems of sprouting and allows uniformity of postharvest germination of seeds. Induction, maintenance, and release of seed dormancy are complex physiological processes that are influenced by a wide range of endogenous and environmental factors. Plant hormones, mainly abscisic acid (ABA) and gibberellin (GA), are the major endogenous factors that act antagonistically in the control of seed dormancy and germination; ABA positively regulates the induction and maintenance of dormancy, while GA enhances germination. Significant progress has been made in recent years in the elucidation of molecular mechanisms regulating ABA/GA balance and thereby dormancy and germination in cereal seeds, and this review summarizes the current state of knowledge on the topic.

Keywords: abscisic acid; cereals; dormancy; germination; gibberellin; plant hormones; preharvest sprouting; seed.

FIGURE 1

Abscisic acid metabolism and signaling pathway in plants. ZEP, zeaxanthin epoxidase; NCED, 9-cis-epoxycarotenoid dioxygenase; ABA2, ABA deficient 2 (short chain alcohol dehydrogenase); AAO3, abscisic aldehyde oxidase; CYP707A1, a cytochrome P450 monooxygenase gene encoding ABA-8′-hydroxylases; PA, phaseic acid; PYR/PYL/RCAR, pyrabactin resistance/pyrabactin-like/regulatory components of ABA receptors; PP2C, protein phosphatase 2C; SnRK2, SNF1-related protein kinase2; ABI3, abscisic acid insensitive 3; ABI4, abscisic acid insensitive 4; ABI5, abscisic acid insensitive 5; VP1, viviparous 1; ABF, ABRE binding factor.

FIGURE 2

Gibberellin metabolism and signaling pathway in plants (GA₁ is the major bioactive GA in seeds of cereals such as wheat). GGDP, geranylgeranyl diphosphate; CDP, ent-copalyl diphosphate; CPS, ent-copalyl diphosphate synthase; KS, ent-kaurene synthase; KO, ent-kaurene oxidase; KAO, ent-kaurenoic acid oxidase; GA20ox, GA20 oxidase; GA3ox, GA3 oxidase; GA2ox, GA2 oxidase; GID1, gibberellin insensitive dwarf 1; GID2, gibberellin insensitive dwarf 2; SLN, slender1 in barley; SLR1, slender rice1; RHT, reduced height; GAMYB, GA regulated MYB transcriptional regulator; KGM, kinase associated with GAMYB.

FIGURE 3

Genetic/molecular elements implicated in the regulation of ABA/GA balance and seed transition between dormancy and germination. ABA inhibits GAMYB-mediated GA responses through modulating the expression of WRKY transcription factors (Xie et al., 2006). DELLA protein regulates the balance between GA and ABA responses, and thereby seed dormancy and germination through its interaction with XERICO, a RING-H2 zinc finger E3 ubiquitin ligase. In the absence of GA, DELLA induces the expression of XERICO, which in turn enhances ABA accumulation, and ABI5 activity (Piskurewicz et al., 2008), leading to dormancy maintenance/inhibition of seed germination. MOTHER OF FT AND TF1 (MFT) represses ABI5 and therefore ABA signaling through a negative feedback mechanism (Xi et al., 2010). The role of MFT in regulating the balance between ABA and GA responses and thereby seed dormancy and germination involves ABI3 and ABI5 that act as repressor and activator of MFT expression, respectively, and DELLA that acts as activator of MFT expression (Xi et al., 2010). DELAY OF GERMINATION1 (DOG1) regulates ABA signaling and therefore seed dormancy through its interaction with PP2C (Née et al., 2017), and likely through modulating the expression of ABI5 and interacting with ABI3 (Dekkers et al., 2016). DOG1 also regulates GA metabolism through the expressions of GA biosynthetic and inactivation genes in temperature dependent manner (Kendall et al., 2011; Graeber et al., 2014). SnRK2/PKABA1 binds to GAMYB and repress its transcription (Gómez-Cadenas et al., 2001). See the legends of Figure 1 and Figure 2 for descriptions of ABA and GA signaling components.