DELLA-mediated cotyledon expansion breaks coat-imposed seed dormancy

Seed dormancy is a key adaptive trait in plants responsible for the soil seed bank. The long established hormone-balance theory describes the antagonistic roles of the dormancy promoting plant hormone abscisic acid (ABA), and the germination promoting hormone gibberellin (GA) in dormancy control. Light, temperature, and other dormancy-breaking signals function to modulate the synthesis and perception of these hormones in the seed. However, the way in which these hormones control dormancy in the imbibed seed remains unknown. Here, we show that the DELLA protein regulators of the GA response are required for dormancy and describe a model through which hormone signal integration and dormancy regulation is achieved. We demonstrate that cotyledon expansion precedes radicle emergence during Arabidopsis seed germination and that a striking correlation exists between final seedling cotyledon size and seed dormancy in the DELLA mutants. Furthermore, twelve previously characterized seed-dormancy mutants are also defective in the control of cotyledon size in a manner consistent with their effect on germination potential. We propose that DELLA-mediated, light-, temperature-, and hormone-responsive cotyledon expansion prior to radicle emergence overcomes dormancy imposed by the seed coat and underlies seed-dormancy control in Arabidopsis.     

Dormancy of Medicago marina (L.) seed

Medicago marina (L.) is a Mediterranean species whose seeds show strong dormancy that prevents germination. We used an integrated approach of physiological analyses and proteomics to investigate the mechanisms that control M. marina dormancy/germination and that underlie stress tolerance. First, we evaluated the effects on dormancy breaking of the following treatments: mechanical scarification, freezing at −20 °C, storage for 4 months and heating at 100 °C for 1 h. Mechanical scarification and freezing were the most effective treatments in overcoming dormancy. The role of abscisic acid (ABA) in M. marina dormancy was studied by ELISA immuno-enzymatic assay. The ABA content of germinated and non-germinated mature (control) and treated seeds was determined. The level of ABA was higher in treated seeds than in control seeds; the most significant increase occurred in the heated seeds. A comparison of the ABA level in the germinated, control and treated seeds suggests that different mechanisms modulate ABA content in response to different stresses, and that a specific ABA-signalling pathway regulates germination. Proteomic analysis revealed 46 proteins differentially expressed between treated and untreated seeds; 14 of these proteins were subsequently identified by mass spectrometry. Several of the proteins identified are important factors in the stress response, and are involved in such diverse functions as lipid metabolism, protein folding and chromatin protection. Lastly, an analysis of the phosphoproteome maps showed that the function of many proteins in seeds subjected to temperature treatment is modulated through post-translational modifications.     

The Arabidopsis COMATOSE locus regulates germination potential

Mutation of the COMATOSE locus in Arabidopsis results in a marked reduction in germination potential. Whilst the morphology of comatose (cts) embryos is not altered, physiological analysis reveals that mature cts seeds do not respond to gibberellin. Prolonged chilling of imbibed seeds only partially restores germination potential, and seeds do not after ripen. Genetic analysis shows that the cts phenotype is expressed in the embryo and phenotypic differences between wild-type and mutant plants were not observed during other stages of plant growth and development. Therefore cts represents a new class of mutant, with a specific lesion that results in severely impaired germination potential. Genetic interactions were analysed between cts and loci that regulate embryo maturation, and abscisic acid biosynthesis and perception. Results from these studies showed that the cts mutant phenotype required the wild-type action of these loci, and suggested that CTS exerts a repressive function on these loci. A model is presented postulating that CTS promotes increased germination potential, and represses embryo dormancy. These functions of CTS may result in the removal of embryo dormancy as a prerequisite to germination.     

The Time Required for Dormancy Release in Arabidopsis Is Determined by DELAY OF GERMINATION1 Protein Levels in Freshly Harvested Seeds

Seed dormancy controls the start of a plant's life cycle by preventing germination of a viable seed in an unfavorable season. Freshly harvested seeds usually show a high level of dormancy, which is gradually released during dry storage (after-ripening). Abscisic acid (ABA) has been identified as an essential factor for the induction of dormancy, whereas gibberellins (GAs) are required for germination. The molecular mechanisms controlling seed dormancy are not well understood. DELAY OF GERMINATION1 (DOG1) was recently identified as a major regulator of dormancy in Arabidopsis thaliana. Here, we show that the DOG1 protein accumulates during seed maturation and remains stable throughout seed storage and imbibition. The levels of DOG1 protein in freshly harvested seeds highly correlate with dormancy. The DOG1 protein becomes modified during after-ripening, and its levels in stored seeds do not correlate with germination potential. Although ABA levels in dog1 mutants are reduced and GA levels enhanced, we show that DOG1 does not regulate dormancy primarily via changes in hormone levels. We propose that DOG1 protein abundance in freshly harvested seeds acts as a timer for seed dormancy release, which functions largely independent from ABA.     

Seed dormancy and ABA signaling: The breakthrough goes on

The seed is an important organ in higher plants, it is an important organ for plant survival and species dispersion. The transition between seed dormancy and germination represents a critical stage in the plant life cycle and it is an important ecological and commercial trait. A dynamic balance of synthesis and catabolism of two antagonistic hormones, abscisic acid (ABA) and giberellins (GAs), controls the equilibrium between seed dormancy and germination. Embryonic ABA plays a central role in induction and maintenance of seed dormancy and also inhibits the transition from embryonic to germination growth. Therefore, the ABA metabolism must be highly regulated at both temporal and spatial levels during phase of dessication tolerance. On the other hand, the ABA levels do not depend exclusively on the seeds because sometimes it becomes a strong sink and imports it from the roots and rhizosphere through the xylem and/or phloem. These events are discussed in depth here. Likewise, the role of some recently characterized genes belonging to seeds of woody species and related to ABA signaling are also included. Finally, although four possible ABA receptors have been reported, not much is known about how they mediate ABA signaling transduction. However, new publications seem to show that almost all these receptors lack several properties to consider them as such.Key words: ABA/GA balance, ABA in woody plants, ABA-receptors, biosynthetic ABA mutants, rhizosphere ABA, seed dormancy     

生长素调控种子的休眠与萌发

植物种子的休眠与萌发,是植物生长发育过程中的关键阶段,也是生命科学领域的研究热点。种子从休眠向萌发的转换是极为复杂的生物学过程,由外界环境因子、体内激素含量及信号传导和若干关键基因协同调控。大量研究表明,植物激素脱落酸(Abscisic acid, ABA)和赤霉素(Gibberellin acid, GA)是调控种子休眠水平,决定种子从休眠转向萌发的主要内源因子。ABA与GA在含量和信号传导两个层次上的精确平衡,确保了植物种子能以休眠状态在逆境中存活,并在适宜的时间启动萌发程序。生长素(Auxin)是经典植物激素之一,其对向性生长和组织分化等生物学过程的调控已有大量研究。但最近有研究证实,生长素对种子休眠有正向调控作用,这表明生长素是继ABA之后的第二个促进种子休眠的植物激素。本文在回顾生长素的发现历程、阐释生长素体内合成途径及信号传导通路的基础上,重点综述了生长素通过与ABA的协同作用调控种子休眠的分子机制,并对未来的研究热点进行了讨论和展望。     

脱落酸调控种子休眠和萌发的分子机制

脱落酸(ABA)是调控种子休眠和萌发过程的主要植物激素。种子内源ABA含量和种胚对ABA敏感性共同调控种子休眠和萌发过程, 确保植物种子以休眠状态在逆境中保持其自身繁衍能力, 并在适宜的环境下启动萌发程序。种子ABA合成代谢和ABA信号转导途径涉及许多重要基因家族, 它们通过复杂的调控网络精确地控制着种胚发生、种子成熟、休眠及萌发进程。该文对ABA调控种子休眠和萌发的分子机制最新研究进展进行综述, 并展望了今后的研究方向。     

S-Nitrosoglutathion Reductase Activity Modulates the Thermotolerance of Seeds Germination by Controlling ABI5 Stability under High Temperature

Seed germination or dormancy status is strictly controlled by endogenous phytohormone and exogenous environment signals. Abscisic acid (ABA) is the important phytohormone to suppress seed germination. Ambient high temperature (HT) also suppressed seed germination, or called as secondary seed dormancy, through upregulating ABI5, the essential component of ABA signal pathway. Previous result shows that appropriate nitric oxide (NO) breaks seed dormancy through triggering S-nitrosoglutathion reductase (GSNOR1)-dependent S-nitrosylation modification of ABI5 protein, subsequently inducing the degradation of ABI5. Here we found that HT induced the degradation of GSNOR1 protein and reduced its activity, thus accumulated more reactive nitrogen species (RNS) to damage seeds viability. Furthermore, HT increased the S-nitrosylation modification of GSNOR1 protein, and triggered the degradation of GSNOR1, therefore stabilizing ABI5 to suppress seed germination. Consistently, the ABI5 protein abundance was lower in the transgenic line overexpressing GSNOR1, but higher in the gsnor mutant after HT stress. Genetic analysis showed that GSNOR1 affected seeds germination through ABI5 under HT. Taken together, our data reveals a new mechanism by which HT triggers the degradation of GSNOR1, and thus stabilizing ABI5 to suppress seed germination, such mechanism provides the possibility to enhance seed germination tolerance to HT through genetic modification of GNSOR1.     

Immunolocalization of FsPK1 correlates this abscisic acid-induced protein kinase with germination arrest in Fagus sylvatica L. seeds

An enzymatically active recombinant protein kinase, previously isolated and characterized in Fagus sylvatica L. dormant seeds (FsPK1), was used to obtain a specific polyclonal antibody against this protein. Immunoblotting and immunohistochemical analysis of FsPK1 protein in beech seeds showed a strong immunostaining in the nucleus of the cells located in the vascular tissue of the embryonic axis corresponding to the future apical meristem of the root. This protein kinase was found to accumulate in the seeds only when embryo growth was arrested by application of ABA, while the protein amount decreased during stratification, previously proved to alleviate dormancy, and no protein was detected at all when seed germination was induced by addition of GA(3). These results indicate that FsPK1 may be involved in the control of the embryo growth mediated by ABA and GAs during the transition from dormancy to germination in Fagus sylvatica seeds.     

Dormancy release, ABA and pre-harvest sprouting

Seed dormancy is an adaptive trait that enables the seeds of many species to remain quiescent until conditions become favorable for germination. Dormancy is normally initiated during seed maturation and maintained to seed maturity. In mature seeds, the loss of dormancy may be gradual (after-ripening) or can be terminated by chilling and other environmental triggers. Dormancy is an important trait for many important crop species: it inhibits pre-harvest spouting or vivipary, a widespread problem in many regions of the world. Too much dormancy, however, can lead to non-uniform germination in the field. Recent progress has been made in understanding the role of abscisic acid metabolism and dormancy release in both model plants and crop species. Advances in our understanding of the molecular mechanisms that are involved in dormancy, along with approaches using quantitative genetics, will provide new strategies through which the desired level of dormancy can be introduced into crop species.     

The role of light in regulating seed dormancy and germination

Seed dormancy is an adaptive trait in plants. Breaking seed dormancy determines the timing of germination and is, thereby essential for ensuring plant survival and agricultural production. Seed dormancy and the subsequent germination are controlled by both internal cues (mainly hormones) and environmental signals. In the past few years, the roles of plant hormones in regulating seed dormancy and germination have been uncovered. However, we are only beginning to understand how light signaling pathways modulate seed dormancy and interaction with endogenous hormones. In this review, we summarize current views of the molecular mechanisms by which light controls the induction, maintenance and release of seed dormancy, as well as seed germination, by regulating hormone metabolism and signaling pathways.     

光信号与激素调控种子休眠和萌发研究进展

休眠是种子植物在长期进化过程中产生的适应性性状, 通过抑制种子在不适宜的环境中萌发进而保证植物能够在逆境中生存。此外, 休眠有助于种子的长距离运输和扩散, 因此休眠对种子延续和物种保存具有重要意义。种子由休眠向萌发的发育转变不仅关系到物种的繁衍, 而且对保证农业生产中作物的产量和品质也具有重要作用。种子的休眠和萌发受到内源激素和外源光信号的共同调控。其中, 外源光信号主要通过调控内源ABA和GA的生物合成及信号转导进而调控种子休眠和萌发。该文系统综述了外源光信号和内源激素调控种子休眠和萌发的作用通路以及两类信号通路之间的交互作用, 旨在为农业生产中利用光和激素调控种子休眠与萌发提供参考。     

光信号与激素调控种子休眠和萌发研究进展

休眠是种子植物在长期进化过程中产生的适应性性状, 通过抑制种子在不适宜的环境中萌发进而保证植物能够在逆境中生存。此外, 休眠有助于种子的长距离运输和扩散, 因此休眠对种子延续和物种保存具有重要意义。种子由休眠向萌发的发育转变不仅关系到物种的繁衍, 而且对保证农业生产中作物的产量和品质也具有重要作用。种子的休眠和萌发受到内源激素和外源光信号的共同调控。其中, 外源光信号主要通过调控内源ABA和GA的生物合成及信号转导进而调控种子休眠和萌发。该文系统综述了外源光信号和内源激素调控种子休眠和萌发的作用通路以及两类信号通路之间的交互作用, 旨在为农业生产中利用光和激素调控种子休眠与萌发提供参考。     

A role for brassinosteroids in germination in Arabidopsis

This paper presents evidence that plant brassinosteroid (BR) hormones play a role in promoting germination. It has long been recognized that seed dormancy and germination are regulated by the plant hormones abscisic acid (ABA) and gibberellin (GA). These two hormones act antagonistically with each other. ABA induces seed dormancy in maturing embryos and inhibits germination of seeds. GA breaks seed dormancy and promotes germination. Severe mutations in GA biosynthetic genes in Arabidopsis, such as ga1-3, result in a requirement for GA application to germinate. Whereas previous work has shown that BRs play a critical role in controlling cell elongation, cell division, and skotomorphogenesis, no germination phenotypes have been reported in BR mutants. We show that BR rescues the germination phenotype of severe GA biosynthetic mutants and of the GA-insensitive mutant sleepy1. This result shows that BR stimulates germination and raises the possibility that BR is needed for normal germination. If true, we would expect to detect a germination phenotype in BR mutants. We found that BR mutants exhibit a germination phenotype in the presence of ABA. Germination of both the BR biosynthetic mutant det2-1 and the BR-insensitive mutant bri1-1 is more strongly inhibited by ABA than is germination of wild type. Thus, the BR signal is needed to overcome inhibition of germination by ABA. Taken together, these results point to a role for BRs in stimulating germination.