The level of abscisic acid ( ABA abscisic acid ) in any particular tissue in a plant is determined by the rate of biosynthesis and catabolism of the hormone. Therefore, identifying all the genes involved in the metabolism is essential for a complete understanding of how this hormone directs plant growth and development. To date, almost all the biosynthetic genes have been identified through the isolation of auxotrophic mutants. On the other hand, among several ABA catabolic pathways, current genomic approaches revealed that Arabidopsis CYP707A genes encode ABA 8′-hydroxylases, which catalyze the first committed step in the predominant ABA catabolic pathway. Identification of ABA metabolic genes has revealed that multiple metabolic steps are differentially regulated to fine-tune the ABA level at both transcriptional and post-transcriptional levels. Furthermore, recent ongoing studies have given new insights into the regulation and site of ABA metabolism in relation to its physiological roles.

Summary: The cleavage of 9‐cis‐epoxycarotenoids to xanthoxin, catalyzed by 9‐cis‐epoxycarotenoid dioxygenases, is considered to be the key regulatory step of abscisic acid (ABA) biosynthesis. In Arabidopsis, genes for these enzymes form a multigene family with nine members, only five of which are thought to be involved in ABA production. In contrast to the prominent function of AtNCED3 in stress responses, the physiological and developmental role of the other 9‐cis‐epoxycarotenoid dioxygenases (NCEDs) remain unknown. Our functional and expression analyses have revealed that AtNCED6 and AtNCED9 are required for ABA biosynthesis during seed development. Reverse genetic analysis showed that ABA levels were reduced in Atnced6 and Atnced9 mutant seeds. In addition, transgenic plants overexpressing the AtNCED6 gene overproduced ABA. In accordance with mutant phenotypes, both AtNCED6 and AtNCED9 exhibited seed‐specific expression. Detailed cytological studies were carried out, either by using transcriptional fusions of the promoter with GUS and GFP reporter genes, or by in situ hybridization. Expression of AtNCED6 was observed exclusively in the endosperm during seed development, that of AtNCED9 in both embryo and endosperm at mid‐development. In addition to reduced ABA levels, Atnced6 and Atnced9 mutant seeds were also resistant to paclobutrazol, a gibberellin biosynthesis inhibitor. Although seeds of single mutants were still dormant, reduced dormancy was observed in the Atnced6 Atnced9 double‐mutant seeds. These demonstrate that ABA synthesized in both the endosperm and the embryo participates in the hormonal balance that controls seed dormancy and germination.

Abscisic acid (ABA) is a key hormone that promotes dormancy during seed development on the mother plant and after seed dispersal participates in the control of dormancy release and germination in response to environmental signals. The modulation of ABA endogenous levels is largely achieved by fine-tuning, in the different seed tissues, hormone synthesis by cleavage of carotenoid precursors and inactivation by 8′-hydroxylation. In this review, we provide an overview of the current knowledge on ABA metabolism in developing and germinating seeds; notably, how environmental signals such as light, temperature and nitrate control seed dormancy through the adjustment of hormone levels. A number of regulatory factors have been recently identified which functional relationships with major transcription factors, such as ABA INSENSITIVE3 (ABI3), ABI4 and ABI5, have an essential role in the control of seed ABA levels. The increasing importance of epigenetic mechanisms in the regulation of ABA metabolism gene expression is also described. In the last section, we give an overview of natural variations of ABA metabolism genes and their effects on seed germination, which could be useful both in future studies to better understand the regulation of ABA metabolism and to identify candidates as breeding materials for improving germination properties.

Dormancy is an adaptive trait that enables seed germination to coincide with favorable environmental conditions. It has been clearly demonstrated that dormancy is induced by abscisic acid (ABA) during seed development on the mother plant. After seed dispersal, germination is preceded by a decline in ABA in imbibed seeds, which results from ABA catabolism through 8′-hydroxylation. The hormonal balance between ABA and gibberellins (GAs) has been shown to act as an integrator of environmental cues to maintain dormancy or activate germination. The interplay of ABA with other endogenous signals is however less documented. In numerous species, ethylene counteracts ABA signaling pathways and induces germination. In Brassicaceae seeds, ethylene prevents the inhibitory effects of ABA on endosperm cap weakening, thereby facilitating endosperm rupture and radicle emergence. Moreover, enhanced seed dormancy in Arabidopsis ethylene-insensitive mutants results from greater ABA sensitivity. Conversely, ABA limits ethylene action by down-regulating its biosynthesis. Nitric oxide (NO) has been proposed as a common actor in the ABA and ethylene crosstalk in seed. Indeed, convergent evidence indicates that NO is produced rapidly after seed imbibition and promotes germination by inducing the expression of the ABA 8′-hydroxylase gene, CYP707A2, and stimulating ethylene production. The role of NO and other nitrogen-containing compounds, such as nitrate, in seed dormancy breakage and germination stimulation has been reported in several species. This review will describe our current knowledge of ABA crosstalk with ethylene and NO, both volatile compounds that have been shown to counteract ABA action in seeds and to improve dormancy release and germination.

Abscisic acid (ABA) is an important hormone for seed development and germination whose physiological action is modulated by its endogenous levels. Cleavage of carotenoid precursors by 9-cis epoxycarotenoid dioxygenase (NCED) and inactivation of ABA by ABA 8′-hydroxylase (CYP707A) are key regulatory metabolic steps. In Arabidopsis (Arabidopsis thaliana), both enzymes are encoded by multigene families, having distinctive expression patterns. To evaluate the genome-wide impact of ABA deficiency in developing seeds at the maturation stage when dormancy is induced, we used a nced2569 quadruple mutant in which ABA deficiency is mostly restricted to seeds, thus limiting the impact of maternal defects on seed physiology. ABA content was very low in nced2569 seeds, similar to the severe mutant aba2; unexpectedly, ABA Glc ester was detected in aba2 seeds, suggesting the existence of an alternative metabolic route. Hormone content in nced2569 seeds compared with nced259 and wild type strongly suggested that specific expression of NCED6 in the endosperm is mainly responsible for ABA production. In accordance, transcriptome analyses revealed broad similarities in gene expression between nced2569 and either wild-type or nced259 developing seeds. Gene ontology enrichments revealed a large spectrum of ABA activation targets involved in reserve storage and desiccation tolerance, and repression of photosynthesis and cell cycle. Proteome and metabolome profiles in dry nced2569 seeds, compared with wild-type and cyp707a1a2 seeds, also highlighted an inhibitory role of ABA on remobilization of reserves, reactive oxygen species production, and protein oxidation. Down-regulation of these oxidative processes by ABA may have an essential role in dormancy control.

Cell wall remodeling is an essential mechanism for the regulation of plant growth and architecture, and xyloglucans (XyGs), the major hemicellulose, are often considered as spacers of cellulose microfibrils during growth. In the seed, the activity of cell wall enzymes plays a critical role in germination by enabling embryo cell expansion leading to radicle protrusion, as well as endosperm weakening prior to its rupture. A screen for Arabidopsis (Arabidopsis thaliana) mutants affected in the hormonal control of germination identified a mutant, xyl1, able to germinate on paclobutrazol, an inhibitor of gibberellin biosynthesis. This mutant also exhibited reduced dormancy and increased resistance to high temperature. The XYL1 locus encodes an α-xylosidase required for XyG maturation through the trimming of Xyl. The xyl1 mutant phenotypes were associated with modifications to endosperm cell wall composition that likely impact on its resistance, as further demonstrated by the restoration of normal germination characteristics by endosperm-specific XYL1 expression. The absence of phenotypes in mutants defective for other glycosidases, which trim Gal or Fuc, suggests that XYL1 plays the major role in this process. Finally, the decreased XyG abundance in hypocotyl longitudinal cell walls of germinating embryos indicates a potential role in cell wall loosening and anisotropic growth together with pectin de-methylesterification.