Mature seeds are an ultimate physiological status that enables plants to endure extreme conditions such as high and low temperature, freezing, and desiccation. Seed longevity, the period over which seed remains viable, is an important trait not only for plant adaptation to changing environments, but also for example, for agriculture and conservation of biodiversity. Reduction of seed longevity is often associated with oxidation of cellular macromolecules such as nucleic acids, proteins and lipids. Seeds possess two main strategies to combat these stressful conditions; protection and repair. The protective mechanism includes the formation of glassy cytoplasm to reduce cellular metabolic activities and the production of antioxidants that prevent accumulation of oxidized macromolecules during seed storage. The repair system removes damage accumulated in DNA, RNA and proteins upon seed imbibition through enzymes such as DNA glycosylase and methionine sulfoxide reductase. In addition to longevity, dormancy is also an important adaptive trait that contributes to seed lifespan. Studies in Arabidopsis have shown that the seed-specific transcription factor ABSCISIC ACID-INSENSITIVE3 (ABI3) plays a central role in abscisic acid (ABA)-mediated seed dormancy and longevity. Seed longevity largely relies on the viability of embryos. Nevertheless, characterization of mutants with altered seed coat structure and constituents has demonstrated that although the maternally-derived cell layers surrounding the embryos are dead, they have a significant impact on longevity.

Transmembrane transport of plant hormones is required for plant growth and development. Despite reports of a number of proteins that can transport the plant hormone gibberellin (GA), the mechanistic basis for GA transport and the identities of the transporters involved remain incomplete. Here, we provide evidence that Arabidopsis SWEET proteins, AtSWEET13 and AtSWEET14, which are members of a family that had previously been linked to sugar transport, are able to mediate cellular GA uptake when expressed in yeast and oocytes. A double sweet13 sweet14 mutant has a defect in anther dehiscence and this phenotype can be reversed by exogenous GA treatment. In addition, sweet13 sweet14 exhibits altered long distant transport of exogenously applied GA and altered responses to GA during germination and seedling stages. These results suggest that AtSWEET13 and AtSWEET14 may be involved in modulating GA response in Arabidopsis.

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.

Dry seeds contain translatable, long-lived mRNAs that are stored during seed maturation. Early studies using transcriptional inhibitors supported the view that protein synthesis during the initial phase of germination occurs on long-lived mRNA templates. Rice seeds were treated with the transcriptional inhibitor actinomycin D (Act D), and the embryonic proteins translated from long-lived mRNAs during germination were identified using a proteomic analysis. De novo transcription was not required for germination of rice seeds, since >80% of seeds germinated when transcription was prevented by treatment with Act D. In contrast, germination was completely inhibited in the presence of cycloheximide, an inhibitor of translation. Thus, de novo protein synthesis is necessary for germination of rice seeds. The proteomic analysis revealed that 20 proteins are up-regulated during germination, even after Act D treatment. Many of the up-regulated proteins are involved in carbohydrate metabolism and cytoskeleton formation. These results indicate that some of the germination-specific proteins involved in energy production and maintenance of cell structure in rice seeds are synthesized from long-lived mRNAs. The timing of translation of eight up-regulated proteins was clearly later than that of the other up-regulated proteins under conditions in which transcription was inhibited by Act D, suggesting that translation of long-lived mRNAs in rice seeds is regulated according to the germination phase.

Seeds characteristics such as germination ability, dormancy, and storability/longevity are important traits in agriculture, and various genes have been identified that are involved in its regulation at the transcriptional and post-transcriptional level. A particularity of mature dry seeds is a special mechanism that allows them to accumulate more than 10,000 mRNAs during seed maturation and use them as templates to synthesize proteins during germination. Some of these stored mRNAs are also referred to as long-lived mRNAs because they remain translatable even after seeds have been exposed to long-term stressful conditions. Mature seeds can germinate even in the presence of transcriptional inhibitors, and this ability is acquired in mid-seed development. The type of mRNA that accumulates in seeds is affected by the plant hormone abscisic acid and environmental factors, and most of them accumulate in seeds in the form of monosomes. Release of seed dormancy during after-ripening involves the selective oxidation of stored mRNAs and this prevents translation of proteins that function in the suppression of germination after imbibition. Non-selective oxidation and degradation of stored mRNAs occurs during long-term storage of seeds so that the quality of stored RNAs is linked to the degree of seed deterioration. After seed imbibition, a population of stored mRNAs are selectively loaded into polysomes and the mRNAs, involved in processes such as redox, glycolysis, and protein synthesis, are actively translated for germination.

Seed priming is a commercially used technique for improving seed performance including germination. However, the treatment sometimes reduces seed longevity as a side effect, limiting the storable period or longevity of the seeds. To overcome this problem, molecular mechanisms involved in the loss of seed longevity during priming were analyzed using natural variations of Arabidopsis thaliana. We found that the Est-1 accession retained longevity for longer after priming compared to the reference accession Col-0. QTL analysis using 279 recombinant inbred lines (RILs) derived from the Est-1 × Col-0 detected three QTL regions associated with the loss of seed longevity during priming. Bulked transcriptome analysis (RNA-Seq with bulked RIL populations) revealed that genes related to brassinosteroid (BR) biosynthesis/signaling and cell wall modification were highly expressed in primed seeds with shorter longevity. After priming, BR-deficient mutants cyp85a1/a2 and det2 showed significantly longer longevity than the wild type (WT). Moreover, tetrazolium staining indicated that mutant seed coats were less permeable after priming than those of WT. We suggest that the loss of seed longevity in primed seed is due to increased seed coat permeability, which is positively regulated, at least partly, via BR signaling.