Nội dung

Int.J.Curr.Microbiol.App.Sci (2017) 6(11): 3095-3106 International Journal of Current Microbiology and Applied Sciences ISSN: 2319-7706 Volume 6 Number 11 (2017) pp. 3095-3106 Journal homepage: http://www.ijcmas.com Review Article https://doi.org/10.20546/ijcmas.2017.611.363 Seed Dormancy at Molecular Level N.T. Komala*, R. Gurumurthy and P. Surendra Department of Seed Science and Technology, College of Agriculture, University of Agricultural Sciences, Dharwad, Karnataka, India *Corresponding author ABSTRACT Keywords Seed dormancy, Seed germination, ABA and GA. Article Info Accepted: 24 September 2017 Available Online: 10 November 2017 The seed containing an embryo, a miniature of new plant, structurally and physiologically equipped to sustain the growing seedling until it establish as new plant. Some traits are acquired during evolution for capacity to survive under unfavourable condition. One of such trait is ‘dormancy’, an intrinsic/extrinsic block to germination. The ABA and GA are involved in induction and release of dormancy and it also showed the involvement and complex interaction with other plant hormones such as ethylene, brassinosteriods and reactive oxygen species. The use of transcriptomic and proteomic analysis refined the variation and similarities of the pathways affected by dormancy and germination. It provides a basis for studying the role of individual genes in these pathways. Advances in molecular technology, especially next-generation sequencing, will make it possible to study non model species in depth at the molecular level. Genetic and molecular mechanisms like silencing and over expression help us to induce and release of seed dormancy in many agricultural crop species which enables to farmers to take up sowing at any time. Introduction Dormancy is a genetically inherited trait whose intensity is modified by environment during seed development. Seed dormancy is a condition, where failure of an intact, viable seed to complete germination under favourable conditions (Bewley, 1997). A seed will germinate in an appropriate environmental condition only after it has lost dormancy. Dormancy and germination are complex traits that are controlled by a large number of genes, which are affected by both developmental and environmental factors. Seed dormancy is an important component of plant fitness (Donohue et al., 2005; Huang et al., 2010) that causes a delay of germination until the arrival of a favourable growth season. Too low seed dormancy levels can lead to germination before the start of a favourable growth season, risking seedling mortality. In contrast, high seed dormancy levels delay germination and reduce the length of the growing season (Donohue et al., 2010). Several of the tissues comprising a seed contribute to its final dormancy level. The roles of the plant hormones abscisic acid and gibberellin in the regulation of dormancy and germination have long been recognized. The last decade saw the identification of several additional factors that influence dormancy including dormancy specific genes, chromatin factors and non-enzymatic processes. 3095 Int.J.Curr.Microbiol.App.Sci (2017) 6(11): 3095-3106 levels, seed maturation, hormonal action, dormancy and chromatin regulation. Site of dormancy Dormancy resides in seeds in the two distinct sites. 1. Exogenous dormancy (Embryo coverings) is caused by physical factor: testa, pericarp, perisperm, and endosperm. 2. Endogenous dormancy: Embryo itself, caused by physiological and bio chemical factors. Advantages of seed dormancy As a means of survival to escape adverse or extreme conditions. (Frost, freezing cold temp, prolonged wet or dry periods, desert or drought conditions not fit for survival). As an escape mechanism to ensure distribution and survival in time and space. It is required in certain crops as it prevents vivipary (Groundnut, Maize, Wheat, Soybean etc). Dormant seeds will have longevity (longer shelf life). Disadvantages of seed dormancy Causes practical problems for immediate sowings in crops from freshly harvested seeds (Sunflower, Groundnut) etc. Gives rise to uneven field emergence, plant population and yield etc. Contributes to the occurrence of volunteer plants, weed plants, unwanted crop seeds, leads to field problems. Problem for seed analysis for germination. Seed dormancy breaking treatments are to be imposed. This review gives overall mechanisms that control seed dormancy at the molecular level. Here, the induction and release of dormancy will be discussed along with some case studies in different plant species. Induction of Seed Dormancy The induction of seed dormancy is controlled by a diverse group of regulators that act at various levels and that also show different degrees of specificity. It includes different Seed maturation regulators The stage in seed development and maturation at which dormancy develops varies between species (Bewley and Black, 1994). Seed dormancy can be initiated in mature non-dormant seeds by environmental conditions that do not favor germination (e.g. high temperature and anoxia). Seed development comprises the two major phase’s embryogenesis and seed maturation. Seed dormancy is induced during the seed maturation phase simultaneously with the accumulation of storage compounds, the acquisition of desiccation tolerance and, finally, the quiescence of metabolic activity. Concerted actions of 4 transcription factors, viz., Abscisic Acid Insensitive 3 (ABI3), Fusca 3 (FUS3), Leafy Cotyledon 1 (LEC1) and LEC2, play a central role in the regulation of seed maturation and the phase transition from embryo to seedling. Several factors, which control seed dormancy indirectly by regulating ABI3, FUS3, LEC1and LEC2, have recently been identified. Maize Viviparous 8 (VP8) has been shown to regulate these transcription factors and a mutation in this gene causes a viviparous seed phenotype with pleiotropic developmental changes (Suzuki et al., 2008). All 4 abi3, lec1, lec2 and fus3 mutants are severely affected in seed maturation and share some common phenotypes, such as decreased dormancy at maturation (Raz et al., 2001). It has been shown that ABI3, FUS3, LEC1 and LEC2 interact as a network to control various aspects of seed maturation (Fig. 1). LEC1 was shown to regulate the expression of ABI3 and FUS3 (Kagaya et al., 2005), FUS3 and LEC2 have been shown to act in a partially redundant manner to control gene expression of seed specific proteins, and LEC2 was shown to locally regulate FUS3 expression in 3096 Int.J.Curr.Microbiol.App.Sci (2017) 6(11): 3095-3106 regions of the cotyledons (Kroj et al., 2003). The indication of redundant regulation within this group of genes was recently shown (To et al., 2006). It was found that one of the major roles of LEC2 was to up-regulate FUS3 and ABI3. The lec2 mutation leads to a dramatic decrease in ABI3 and FUS3 expression, and most lec2 phenotypes can be rescued by ABI3 or FUS3 constitutive expression. LEC1 positively regulates ABI3 and FUS3 in the cotyledons (To et al., 2006). Hormonal regulation Several lines of evidence have established that abscisic acid (ABA) induces dormancy during embryo maturation (reviewed in Feurtado and Kermode 2007, Finch-Savage, 2006, Kermode, 2005). In particular, the balance between the levels of ABA and GA hormones and their respective signalling pathways are important in regulating both induction and maintenance of dormancy, and promotion of germination. A recent epochmaking finding concerning ABA was the identification of PYR/PYL/RCAR ABA receptors (Ma et al., 2009; Park et al., 2009). 14 members of this protein family in Arabidopsis function redundantly in mediating the ABA response by interacting with type 2C protein phosphatase (PP2C) negative regulators and antagonizing their action. However, it is not known yet whether any of these PYR/PYL/RCAR proteins are specifically involved in ABA signalling during the seed maturation stage. The PP2Cs ABA-Insensitive 1 (ABI1) and ABI2 were originally identified in ABA-insensitive mutant screen. The abi1-1 and abi2-1 mutants show reduced dormancy phenotypes and are caused by dominant-negative mutations that lead to abi proteins that are unable to bind to the ABA receptors (Ma et al., 2009; Park et al., 2009). In the presence of ABA, these abiPP2Cs remain active and repress downstream ABA-activated protein kinases belonging to the SNF1-related protein kinase subfamily 2 (SnRK2). Three Arabidopsis SnRK2s (SnRK2.2, SnRK2.3 and SnRK2.6) have been shown to act redundantly in the transmission of an ABA signal during seed development and dormancy induction (reviewed by Nambara et al., 2010). The triple mutant of these kinases is nearly blind to ABA and exhibits abnormal seed development, produces ABA-insensitive green seeds similar to severe alleles of abi3 and germinates early under high humidity conditions (Nakashima et al., 2009). Major targets of these kinases have been shown to be a group of bZIP-type transcription factors including ABI5 and Abscisic acid Responsive Elements binding Protein 3 (AREB3). Surprisingly, mutants of these transcription factors generally do not show strong dormancy phenotypes. Antagonistic to ABA action, GA, ethylene and other hormones have been shown to promote germination. Environmental signals such as light and temperature during imbibition and germination are integrated into GA biosynthesis and signalling by transcription factors like Phytochrome Interacting Factor 3-Like 5 (PIL5) and Spatula (SPT). These observations further reinforce the importance of the coordinated interaction of various hormones in the regulation of dormancy and germination. Seed dormancy is an important agronomic trait in cereals. Liu et al., 2014 correlated seed dormancy phenotypes with abscisic acid (ABA) and gibberellin (GA) metabolism gene expression profiles and phytohormone levels during seed development and imbibition. A time course analysis of ABA and GA content during seed development showed that N22 had a high ABA level at early and middle seed developmental stages, while at late developmental stage it declined to the level of ZH11, G46B had the lowest ABA content 3097 Int.J.Curr.Microbiol.App.Sci (2017) 6(11): 3095-3106 during seed development though at early developmental stage its ABA level was close to that of ZH11, and its ABA/GA ratio peaked at late developmental stage that was at the same level of ZH11. Analysis of gene expression in imbibed barley grains shows that the different ABA metabolism genes are targeted by white light and after ripening. Of the genes examined, white light promotes the expression of an ABA biosynthetic gene, HvNCED1, in embryos. Enzyme linked immunosorbent assays (ELISA) showed that dormant grains imbibed under white light have higher embryo ABA content than grains imbibed in the dark. After ripening has no effect on expression of ABA biosynthesis genes, but promotes expression of an ABA catabolism gene (HvABA8’OH1), a GA biosynthetic gene (HvGA3ox2), and a GA catabolic gene (HvGA2ox3) following imbibition (Gubler et al., 2008). Chono et al., 2013 cloned the wheat ABA 8'-hydroxyase gene which was highly expressed during seed development (TaABA8'OHl) and screened for mutations that lead to reduced ABA catabolism. Peach genomic sequencing was accomplished in 2013 (Verde et al., 2013); however, the functions of most of the genes are not clear. Some few genes relating to ABA synthesis and catabolism have been identified. Endo’s method (2014) to deduce the NCEDs, CYP707As, AAOs, ZEP, SDR1 genes in the peach genome sequence (Endo et al., 2014). Seed dormancy-specific genes Only some few genes regulating dormancy have been identified that are not directly involved in hormone metabolism or seed maturation. Two examples are Histone Monoubiqutination1 (HUB1) and Reduced Dormancy 2 (RDO2) in Arabidopsis. The 1st cloned dormancy QTL in Arabidopsis, Delay of Germination 1 (DOG1), encodes a protein of unknown function (Bentsink et al., 2006). The absence of dormancy with no obvious pleiotropic phenotypes in the dog1 mutant indicates that DOG1 is a main player specific for the induction of seed dormancy; dog1 mutants are completely nondormant and do not show any obvious pleiotropic phenotypes, apart from a reduced seed longevity. The DOG1 protein belongs to a small family in Arabidopsis that was recently shown to be conserved in other plant species. DOG1 homologs have been found in the Arabidopsis related species Lepidium sativum and Brassica rapa (Graeber et al., 2010) and in the monocot rice (Oryza sativa; Sugimoto et al., 2010) Extensive QTL mapping has been performed for dormancy/pre-harvest sprouting traits in crop species. Recently, Seed dormancy 4 (Sdr4) has been identified as one of the major determinants for dormancy in rice. Sdr4 is localized in the nucleus and that it affects the expression of several DOG1-LIKE genes (rice genes similar to Arabidopsis DOG1). Its mechanism of action is still not understood because Sdr4 encodes a novel protein with unknown function (Sugimoto et al., 2010). Characterization of the function of these novel factors and the molecular identification of additional dormancy QTLs will provide us with more solution on the mechanisms that control the induction and maintenance of dormancy. The molecular mechanisms of seed dormancy are not well understood. Delay of Germination1 (DOG1) was recently identified as a major regulator of dormancy in Arabidopsis thaliana. Nakabayashi et al., in 2012 showed that the DOG1 protein accumulates during seed maturation and remains stable throughout seed storage and imbibition. The levels of DOG1 protein in newly harvested seeds highly correlate with dormancy. The DOG1 protein becomes modified during after ripening, and its levels 3098 Int.J.Curr.Microbiol.App.Sci (2017) 6(11): 3095-3106 in stored seeds do not correlate with germination potential. Genes involved in the ABA signal transduction pathway also influence seed dormancy. In particular, members of the Protein Phosphatase 2C (PP2C) family were identified as components of ABA signaling from work with the aba insensitive1-1 (abi11) and abi2-1 mutants (Koornneef et al., 1984; Rodriguez et al., 1998). In a mutagenesis screen of a highly dormant Arabidopsis line, the reduced dormancy5 (rdo5) mutant was isolated based on its strongly reduced seed dormancy. The cloning of RDO5 showed that it encodes a PP2C phosphatase. Several PP2C phosphatases belonging to clade A are involved in abscisic acid signaling and control seed dormancy (Xiang et al., 2014). Regulation of dormancy at chromatin level Epigenetics Study of changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself. Change in phenotype without a change in genotype. Molecular basis of epigenetics: Histone modifications Dormancy 2 have been identified in a screen for reduced dormancy mutants (Peeters et al., 2002). Both proteins probably influence seed dormancy by regulating transcription elongation of seed dormancy genes during maturation (Liu et al., 2011). Two other chromatin factors, SIN3-LIKE1 (SNL1) and SNL2, positively regulate seed dormancy by modifying the ABA ethylene antagonism through histone acetylation (Wang et al., 2013). A role for histone acetylation in seed dormancy was recently demonstrated by the reduced dormancy phenotype of the histone deacetylase9 mutant (Van Zanten et al., 2014). The Early Flowering in Short Days (EFS) gene has been selected as a phase transition regulator during seed germination in a transcriptional network modelling study (Bassel et al., 2011). EFS codes for a histone H3 methyltransferase involved in histone H3 lysine 4 trimethylation (H3K4me3), it is a transcription activating histone mark. The KRYPTONITE (KYP)/SUVH4 and SUVH5 genes encode histone methyltransferases that mediate H3K9 dimethylation (Jackson et al., 2002). The kyp-2 and suvh5 mutants show enhanced dormancy and increased expression of several dormancy genes, including DOG1 and ABI3 (Zheng et al., 2012). Release of seed dormancy Is a covalent post-translational modification (PTM) to histone proteins which includes acetylation, methylation, phosphorylation and ubiquitylation. The PTMs made to histones can impact gene expression by altering chromatin structure the organization of chromatin influences gene expression and important for all developmental processes in the plant, including seed dormancy and bud dormancy (Cooke et al., 2012). Dormancy can either be quickly released in imbibed seeds (within a couple of days) or relatively slow in dry seeds (within weeks or months). The molecular mechanisms controlling dormancy release are less well understood compared to that controlling dormancy induction. The fast release of dormancy requires imbibition at species specific temperatures and is called stratification. Histone monoubiquitination 1 and reduced 3099 Int.J.Curr.Microbiol.App.Sci (2017) 6(11): 3095-3106 Fig.1 Interactions in the regulatory network involving LEC1, LEC2, FUS3, and ABI3genes in the control of seed development and maturation Regulation of dormancy at chromatin level In general, imbibition at low temperatures releases dormancy in seeds of summer annuals, while high temperatures release dormancy in seeds of winter annuals. It is largely unclear how stratification drives the release of seed dormancy, and, especially, the temperature sensing mechanism is unknown, but a few genes with a role in this process have been identified. The basic helixloop- helix transcription factors SPT and PIL5 have a role in cold stratification (Pinfield-Wells et al., 2005). SPT is a negative regulator of germination that looses its repressive activity after stratification, whereas PIL5 is not responding to low temperatures, but represses germination in the dark after a cold treatment. Gibberellins (GAs), ethylene, strigolactone, and brassinosteroids influence seed dormancy and germination (Finkelstein et al., 2008; Nelson et al., 2011; Graeber et al., 2012). In general, these hormones reduce seed dormancy and promote seed germination. For example, mutants defective in GA biosynthesis such as ga requiring1 show deep seed dormancy and fail to germinate in the absence of exogenous GA (Debeaujon and Koornneef, 2000; Ogawa et al., 2003). GA treatment alone does not stimulate germination in all species or in fully dormant 3100 Int.J.Curr.Microbiol.App.Sci (2017) 6(11): 3095-3106 Arabidopsis seeds (Ali-Rachedi et al., 2004). A decrease in ABA levels may be required before GA levels and sensitivity can increase (Jacobsen et al., 2002). However, sensitivity to both GA and light increases as after ripening progresses in Arabidopsis and increased GA levels mediate the dormancy relieving effect of moist chilling in Arabidopsis. Light promotes GA synthesis, and light and GA promote the degradation of ABA in imbibing lettuce seeds. The accumulation of the GA biosynthetic gene GA3ox2 (Gibberellin 3 Oxidase) transcript increased 40-fold in after ripened seeds whereas the GA-deactivating enzyme GA2ox1 (Gibberellin 2 Oxidase) was expressed at the highest levels in the highly dormant seeds of Arabidopsis ecotype Cvi (Finch-Savage et al., 2007). Stratification led to increased expression of the GA biosynthesis genes GA20ox1 (Gibberellin 20 Oxidase), GA20ox2, and GA3ox1 and decreased expression of the GA catabolic gene GA2ox2 (Yamauchi et al., 2004). Studies using inhibitors of ethylene biosynthesis or of ethylene action and analysis of mutant lines altered in genes involved in the ethylene signaling pathway (etr1, ein2, ain1, etr1, and erf1) demonstrate the involvement of ethylene in the regulation of germination and dormancy. Ethylene enhances dormancy breaking through interactions with ABA signaling. Ethylene can regulate dormancy by affecting ABA levels and signal transduction (Linkies et al., 2009). For example, induction of thermodormancy at high temperatures is associated with a reduced ethylene production in chickpea (Cicer arietinum; Gallardo et al., 1991), sunflower (Corbineau et al., 1988), and lettuce (Prusinski and Khan, 1990). This decrease in C2H4 production may result from an increase in ACC (1-aminocyclopropane-1carboxylic acid)-malonyltransferase activity, thus from a decrease in ACC content as demonstrated in chickpea (Martinez-Reina et al., 1996), an inhibition of ACO activity (Corbineau et al., 1988; Gallardo et al., 1991), or a reduced expression of ACS (acylCoA synthetase) and ACO (Argyris et al., 2008). Numerous data also suggest that ethylene stimulates seed germination by affecting the GAs biosynthesis or signaling pathway. GA1, GA4, and GA7 strongly accumulate in dry mature seeds of the etr1-2 Arabidopsis mutant relative to wild type, and both GA4 and GA7 contents remain higher than in wild type during the two first days of imbibition (Chiwocha et al., 2005). The changes in GA content during germination suggest that lack of ETR1, i.e., of ethylene signaling pathway, results (i) in alteration of GAs biosynthesis pathway, and (ii) in a requirement for higher levels of GAs than wild type, to promote germination (Chiwocha et al., 2005). In Arabidopsis, Achard et al., (2007) reported that a part of ethylene action on hypocotyl growth and floral transition was mediated via its effects on the DELLA proteins. Ethylene has shown to regulate endosperm cap weakening and rupture in Lepidium sativum, counteracting the action of ABA (Linkies et al., 2009). Very recent reports have demonstrated the roles of strigolactones and karrikins (germination promoting compounds in smoke) in dormancy and germination. Strigolactone signalling is mediated by the F-box protein Karrikin Insensitive 1 (KAI1), strigolactone is allelic to More Axillary Branches 2 (MAX2). The kai1/max2 mutant shows increased primary dormancy (Nelson et al., 2011). It has been shown that strigolactones modulate the ABA/GA ratio in secondary dormancy control (Toh et al., 2012). Brassinosteriods (BRs) are plant steroid hormones involved in stem elongation and leaf unfurling (Clouse, 2001) that also 3101 Int.J.Curr.Microbiol.App.Sci (2017) 6(11): 3095-3106 promote seed germination. In Arabidopsis, epibrassinolide (EBR) and brassinolide (BL) application overcomes nongermination of GA biosynthetic and sleepy 1 (sly1) GA signaling mutants, but BR and GA stimulate tobacco seed germination by different mechanisms (Leubner-Metzger, 2001). The role of reactive oxygen species (ROS) in seed biology has progressively emerged and evolved this last decade. Originally considered as harmful compounds, causing deleterious reactions toward a wide range of biomolecules and to seeds, ROS are now widely acknowledged as signaling compounds regulating the germination process through an hormonal network. Oracz et al., 2007 reported that after-ripening period a progressive accumulation of ROS, namely superoxide anions and hydrogen peroxide, in cells of embryonic axes. Accumulation was investigated at the cellular level by electron microscopy, occurred concomitantly with lipid peroxidation and oxidation (carbonylation) of specific embryo proteins. Incubation of dormant sunflower seeds for 3 h in the presence of hydrogen cyanide (a compound that breaks dormancy) or methylviologen (a ROS-generating compound) also released dormancy and caused the oxidation of a specific set of embryo proteins. Ishibashi et al., (2013) have proposed that ROS produced in soybean (Glycine max) embryonic axes during imbibition induces ethylene production, which promotes cell elongation in the radicle. Nitric oxide (NO), nitrite, and nitrate may stimulate the pentose phosphate pathway, and therefore germination, by increasing oxidation of NADPH to NADP+, a limiting electron acceptor. NO inhibition of catalase may lead to increased accumulation of H2O2 from the βoxidation of stored fatty acids in seeds. Accumulated H2O2 may stimulate germination by acting as a substrate for peroxidases, leading to oxidation of NADPH to NADP+ or by causing breakdown of ABA (Bailly, 2004). In Arabidopsis, NO may stimulate germination by causing vacuolation and cell wall weakening of the aleurone layer (Bethke, 2007). Dormancy and germination are very complex traits under the control of a large number of genes. By understanding seed dormancy at molecular level, we can come to some of the genes which are involved in seed dormancy induction. As we are seed technologist we know that induction of seed dormancy is important in some crops like wheat, barley, ground nut etc. and release of seed dormancy in most of the crops. So genetic and molecular mechanisms create a path to achieve our goal. Genetic and molecular mechanisms like silencing and over expression help us to induce and release of seed dormancy in many agricultural crop species. References Achard, P., Baghour, M., Chapple, A., Hedden, P., Van Der Straeten, D. and Genschik, P., 2007, The plant stress hormone ethylene controls floral transition via DELLAdependent regulation of floral meristemidentity genes. Proc. Natl. Acad. Sci., 104: 6484-6489. Ali-Rachedi, S., Bouinot, D., Wagner, M. H., Bonnet, M. and Sotta, B., 2004, Changes in endogenous abscisic acid levels during dormancy release and maintenance of mature seeds: studies with the Cape Verde Islands ecotype, the dormant model of Arabidopsis thaliana. Planta, 219:479-88. Argyris, J., Dahal, P., Hayashi, E., Still, D.W., and Bradford, K. J., 2008, Genetic variation for lettuce seed thermoinhibition is associated with temperature-sensitive expression of abscisic acid, gibberellin, and ethylene biosynthesis, metabolism, and response genes. Plant Physiol., 148, 926947. Bailly, C., 2004, Active oxygen species and 3102 Int.J.Curr.Microbiol.App.Sci (2017) 6(11): 3095-3106 antioxidants in seed biology. Seed Sci. Res.,14: 93-107. Bassel, G.W., Lan, H., Glaab, E., Gibbs D. J., Gerjets, T., Krasnogor, N., Bonner, A. J., Holdsworth, M. J. and Provart, N. J., 2011, Genome-wide network model capturing seed germination reveals coordinated regulation of plant cellular phase transitions. Proceedings of the National Academy of Sciences of the United States of America. 108: 9709-9714. Bentsink, L., Jowett, J., Hanhart, C. J., and Koornneef, M., 2006, Cloning of DOG1, a quantitative trait locus controlling seed dormancy in Arabidopsis. Proc. Natl. Acad. Sci., 103: 17042-17047. Bethke, P. C., Libourel, I. G., Aoyama, N., Chung, Y. Y., Still, D. W. and Jones R. L., 2007, The Arabidopsis aleurone layer responds to nitric oxide, gibberellin, and abscisic acid and is sufficient and necessary for seed dormancy. Plant Physiol., 143:1173-88. Bewley, J. D and Black, M., 1994, Seeds: physiology of development and germination, New York: Plenum. 367 pp. Bewley, J. D., 1997, Seed germination and dormancy. Plant Cell, 9: 1055-1066. Chiwocha, S. D. S., Cutler, A. J., Abrams, S. R., Ambrose, S. J., Yang, J., and Kermode, A. R., 2005, The ert1-2 mutation in Arabidopsis thaliana affects the abscisic acid, auxin, cytokinin and gibberellin metabolic pathways during maintenance of seed dormancy, moist-chilling and germination. Plant J. 42, 35-48. Chono, M., Matsunaka, H., Seki, M., Fujita, M., Otobe, C. K., Oda, S., Kojima, H., Kobayashi, D. and Kawakami, N., 2013, Isolation of a wheat (Triticum aestivum L.) mutant in ABA 8'-hydroxylase gene:effect of reduced ABA catabolism on germination inhibition under field condition. Breeding Sci., 63: 104-115. Clouse, S., 2001, Brassinosteroids. Curr. Biol. 11:R904. Cooke, J. E. K., Eriksson, M. E. and Junttila, O., 2012, The dynamic nature of bud dormancy in trees: environmental control and molecular mechanisms. Plant, Cell Environ., (In press). Corbineau, F., Rudnicki, R. M., and Come, D., 1988, Induction of secondary dormancy in sunflower seeds by high temperature. Possible involvement of ethylene biosynthesis. Physiol. Plant., 73: 368-373. Debeaujon, I. and Koornneef, M., 2000, Gibberellin requirement for Arabidopsis seed germination is determined both by testa characteristics and embryonic abscisic acid. Plant Physiol., 122: 415-424. Donohue, K., Dorn, L., Griffith, C., Kim, E., Aguilera, A., Polisetty, C. R. and Schmitt, J., 2005, Environmental and genetic influences on the germination of Arabidopsis thaliana in the field. Evolution., 59: 740-757. Donohue, K., Rubio de Casas, R., Burghardt, L., Kovach, K. and Willis, C. G., 2010, Germination, postgermination adaptation, and species ecological ranges. Annual Review of Ecology, Evolution, and Systematics, 41: 293-319. Endo, A., Nelson, K. M., Thoms, K., Abrams, S. R., Nambara, E., and Sato, Y., 2014, Functional characterization of xanthoxin dehydrogenase in rice. J. Plant Physiol., 171: 1231-1240. Feurtado, J. and Kermode, A., 2007, A merging of paths: abscisic acid and hormonal cross-talk in the control of seed dormancy maintenance and alleviation. See Ref., 20: 176-223. Finch-Savage, W. E., Cadman, C. S., Toorop, P. E., Lynn, J. R. and Hilhorst, H. W., 2007, Seed dormancy release in Arabidopsis Cvi by dry after-ripening, low temperature, nitrate and light shows common quantitative patterns of gene expression directed by environmentally specific sensing. Plant J. 51:60-78. Finch-Savage, W. E., Leubner-Metzger, G., 2006, Seed dormancy and the control of germination. New Phytol. 171:501-23. Finkelstein, R., Reeves, W., Ariizumi, T., and Steber, C., 2008, Molecular aspects of seed dormancy. Annu. Rev. Plant Biol., 59: 387415. Gallardo, M., Del Mar Delgado, M., SanchezCalle, I. M., and Matilla, A. J., 1991, Ethylene production and 1aminocyclopropane-1-carboxylic acid 3103 Int.J.Curr.Microbiol.App.Sci (2017) 6(11): 3095-3106 conjugation in thermoinhibited Cicer arietinum L. seeds. Plant Physiol., 97, 122127. Graeber, K., Linkies, A., Müller, K., Wunchova, A., Rott, A., and Leubner-Metzger, G., 2010, Cross-species approaches to seed dormancy and germination: Conservation and biodiversity of ABA regulated mechanisms and the Brassicaceae DOG1 genes. Plant Mol. Biol., 73: 67-87. Graeber, K., Nakabayashi, K., Miatton, E., Leubner-Metzger, G., and Soppe, W. J. J., 2012, Molecular mechanisms of seed dormancy. Plant Cell Environ., 35: 17691786. Gubler, F., Hughes, T., Waterhouse, P. and Jacobsen, J., 2008, Regulation of Dormancy in Barley by Blue Light and After-Ripening: Effects on Abscisic Acid and Gibberellin Metabolism. Plant Physiol., 107:115-469. Huang, X., Schmitt, J., Dorn, L., Griffiths, C., Effgen, S., Takao, S., Koornneef, M. and Donohue, K., 2010, The earliest stages of adaptation in an experimental plant population: strong selection on QTLs for seed dormancy. Molecular Ecology, 19: 1335-1351. Ishibashi, Y., Koda, Y., Zheng, S.-H., Yuasa, T., and Iwaya-Inoue, M., 2013, Regulation of soybean seed germination through ethylene production in response to reactive oxygen species. Ann. Bot., 111: 95-102. Jackson, J. P., Lindroth, A. M., Cao, X. and Jacobsen, S. E., 2002, Control of CpNpG DNA methylation by KRYPTONITE histone H3 methyltransferase. Nature, 416: 556-560. Jacobsen, J. V., Pearce, D. W., Poole, A. T., Pharis, R. P. and Mander, L. N., 2002, Abscisic acid, phaseic acid and gibberellin contents associated with dormancy and germination in barley. Physiol. Plant, 115:428-41. Kagaya, Y., Toyoshima, R., Okuda, R., Usui, H., Yamamoto, A., and Hattori, T., 2005, LEAFY COTYLEDON1 controls seed storage protein genes through its regulation of FUSCA3 and ABSCISIC ACID INSENSITIVE3. Plant Cell Physiol., 46: 399-406. Kermode, A. R., 2005, Role of abscisic acid in seed dormancy. J. Plant Growth Regul., 24:319-44. Koornneef, M., Reuling, G., and Karssen, C. M., 1984, The isolation and characterization of abscisic-acid insensitive mutants of Arabidopsis thaliana. Physiol. Plant., 61: 377-383. Kroj, T., Savino, G., Valon, C., Giraudat, J., and Parcy, F., 2003, Regulation of storage protein gene expression in Arabidopsis. Development, 130: 6065-6073. Leubner-Metzger, G., 2001, Brassinosteroids and gibberellins promote tobacco seed germination by distinct pathways. Planta 213:758-63. Linkies, A., Müller, K. and Morris, K., 2009, Ethylene interacts with abscisic acid to regulate endosperm rupture during germination: a comparative approach using Lepidium sativum and Arabidopsis thaliana. The Plant Cell, 21: 3803-3822. Linkies, A., Muller, K., Morris, K., Tureckova, V., Wenk, M., Cadman, C.S.C., Corbineau, F., Strnad, M., Lynn, J.R., Finch-Savage, W.E., and Leubner-Metzger, G., 2009, Ethylene interacts with abscisic acid to regulate endosperm rupture during germination: a comparative approach using Lepidium sativum and Arabidopsis thaliana. Plant Cel,l 21: 3803-3822. Liu, Y., Geyer, R., van Zanten, M., Carles, A., Li, Y., Horold, A., Nocker, S., and Soppe, W. J. J., 2011, Identification of the Arabidopsis REDUCED DORMANCY 2 gene uncovers a role for the polymerase associated factor 1 complex in seed dormancy. PLoS ONE, 6: e22241. Liu, Y., Fang, J., Xu, F., Chu, J., Yan, C., Schlappi, M. R., Wang, Y. and Chu, C., 2014, Expression patterns of ABA and GA metabolism genes and hormone levels during rice seed development and imbibition: a comparison of dormant and non-dormant rice cultivars. J Genet Genomics, 20; 41(6): 327-38. Ma, Y., Szostkiewicz, I., Korte, A., Moes, D., Yang, Y., Christmann, A. and Grill, E., 2009, Regulators of PP2C phosphatase activity function as abscisic acid sensors. Sci., 324: 1064-1068. Martinez-Reina, G., Matilla, A. J., Martin- 3104