Seed dormancy is a developmental physiological state in which viable seeds fail to germinate despite exposure to conditions that would normally promote germination in nondormant seeds of the same species, serving as a critical survival mechanism that allows seeds to endure adverse environmental periods such as drought, cold, or unsuitable seasons.[1] This temporary inhibition ensures that germination is timed appropriately for optimal seedling establishment, enhancing plant fitness and population persistence.[2]Seed dormancy manifests in various forms, broadly categorized as physiological dormancy (PD), the most common type occurring in approximately 60% of angiosperm species and involving internal regulatory mechanisms within the embryo or endosperm; physical dormancy (PY), resulting from impermeable seed coats that block water or oxygen uptake; and morphological dormancy (MD), where the embryo is underdeveloped and requires additional growth time before germination can proceed.[1][3] Combinations of these types, such as morphophysiological dormancy (MPD), also occur, particularly in species adapted to complex habitats like temperate montane peatlands.[4] These classifications, originally proposed by Nikolaeva and refined by Baskin and Baskin, reflect adaptations to diverse ecological niches.[1][5]At the molecular and hormonal levels, dormancy is primarily governed by the antagonistic interaction between abscisic acid (ABA), which inhibits germination by maintaining embryo quiescence and promoting inhibitor synthesis, and gibberellins (GA), which stimulate embryo growth and cell wall loosening to break dormancy. Recent research as of 2025 has identified additional regulators like long noncoding RNAs in dormancy release.[1][6] Key genes such as DOG1 (Delay Of Germination 1) quantitatively control dormancy depth, while transcription factors like ABI3 and environmental sensors integrate cues such as light, temperature, and after-ripening (dry storage) to modulate ABA:GA ratios.[1] Physical dormancy mechanisms involve specialized seed coat structures, like the strophiole or palisade layer, that must be disrupted through scarification or microbial action for permeability to be restored.[3]Ecologically, seed dormancy evolved as an ancestral trait in seed plants, acting as an "evolutionary hub" that facilitates adaptation to unpredictable environments by forming persistent soil seed banks and preventing mass germination events that could lead to seedling mortality.[7] In agricultural contexts, it poses both challenges and opportunities: strong dormancy can delay crop establishment and reduce yields if not managed through stratification or chemical treatments, but it also protects against pre-harvest sprouting in cereals like wheat, safeguarding grain quality.[2] Understanding and manipulating dormancy remains essential for sustainable farming, restoration ecology, and conserving biodiversity in changing climates.[4]
Fundamentals
Definition
Seed dormancy is defined as a temporary failure of a viable seed to germinate, even when exposed to conditions that are otherwise suitable for germination, such as adequate moisture, oxygen, and temperature. This state represents an endogenous block to germination that persists until specific environmental or physiological cues release it. The classification system for seed dormancy, which underpins this definition, was formalized by Baskin and Baskin in 2004, building on earlier frameworks to encompass various dormancy classes based on the underlying mechanisms and requirements for breaking dormancy.[8]A key distinction exists between seed dormancy and quiescence: dormancy involves an internal, genetically programmed inhibition of germination that cannot be immediately overcome by favorable conditions alone, whereas quiescence is a reversible suspension of germination caused solely by external limitations, such as insufficient water or suboptimal temperature, which dissipates once those conditions improve. Dormancy ensures that seeds do not germinate prematurely, promoting survival under variable environmental conditions.[9]The basic physiological state of dormancy typically arises from one or more factors, including underdeveloped or immature embryos, the presence of chemical inhibitors within the seed tissues, or physical barriers like impermeable seed coats that restrict water imbibition or oxygen diffusion. These mechanisms collectively prevent metabolic processes essential for germination from proceeding. Seed dormancy is prevalent across vascular plants, affecting seeds of approximately 70% of angiosperm species worldwide.[10]The concept of seed dormancy was first systematically explored and described by Crocker in 1916, who identified it as a critical adaptive trait involving inhibitory factors in seeds. A foundational modern synthesis came from Nikolaeva in 1969, who classified dormancy based on physiological and morphological criteria, influencing subsequent research. This framework was refined and expanded by Baskin and Baskin in 2004, with further revisions in 2021 to account for greater diversity in dormancy types observed across species.[11][12]
Evolutionary and Ecological Role
Seed dormancy evolved as a bet-hedging strategy that enables plants to delay germination in response to unfavorable environmental conditions, thereby mitigating the risk of seedling mortality and enhancing long-term reproductive success in unpredictable habitats.[13] This adaptive trait is particularly prominent in angiosperms, whose radiation began around 140 million years ago during the Early Cretaceous, with fossil evidence from that period revealing tiny, underdeveloped embryos consistent with dormancy mechanisms that promoted survival amid fluctuating paleoenvironments.[14]Ecologically, seed dormancy facilitates population persistence by establishing persistent soil seed banks, which serve as vital reservoirs for regenerating plant communities following disturbances and buffering against climatic variability.[15] It synchronizes germination with reliable seasonal cues, such as temperature shifts or moisture availability, ensuring that seedlings emerge during periods conducive to establishment and growth.[13] In regions with erratic weather patterns, this temporal spread of germination events further bolsters species survival by avoiding mass reproductive failures.[16]Representative examples illustrate these benefits: desert-adapted species often exhibit physical dormancy, where impermeable seed coats prevent germination until scarce rainfall events provide the necessary hydration, enabling opportunistic colonization in arid ecosystems.[17] In contrast, many annual plants in fire-prone habitats rely on physiological dormancy, which is released by post-fire cues like smoke or heat, promoting rapid regeneration and community recovery after disturbances.[18]A 2021 revision of seed dormancy classification by Baskin and Baskin highlights the profound role of dormancy in driving phylogenetic diversity, with varied dormancy types documented across more than 300 seed plant families, underscoring its contribution to evolutionary diversification and ecological resilience.[12][10]
Primary Seed Dormancy
Physiological Dormancy
Physiological dormancy (PD) represents the most prevalent form of primary seed dormancy, affecting approximately 70% of species that exhibit dormancy. It arises from internal physiological constraints within the mature embryo or endosperm that inhibit germination, even under otherwise suitable environmental conditions, primarily due to low embryo growth potential or reduced sensitivity to cues like light, temperature, and hormones.[19] Unlike physical dormancy, PD lacks any structural barrier to water uptake, such as an impermeable seed coat.[20]PD is subdivided into three levels—non-deep, intermediate, and deep—based on the duration and type of treatments required to alleviate dormancy, as well as the embryo's response to exogenous gibberellic acid (GA). Non-deep PD, the most common subtype, features seeds where dormancy can be broken through after-ripening via dry storage or brief moist coldstratification (typically 1–3 weeks at 5°C), and GA often promotes germination of excised embryos.[19] This level involves a relatively shallow inhibition, often linked to an imbalance in abscisic acid (ABA) and GA levels that sensitizes seeds to environmental triggers. Representative examples include seeds of tobacco (Nicotiana tabacum), which lose dormancy after several months of dry storage, and cereals such as wheat (Triticum aestivum), where after-ripening shifts the temperature range for germination to favor spring emergence.[21]Intermediate PD requires more prolonged cold stratification (4–13 weeks) to release dormancy, with GA showing limited efficacy in promoting germination of intact seeds, though excised embryos may respond.[19] This level ensures germination aligns with seasonal changes, such as post-winter warming. Seeds of Arabidopsis thaliana exemplify this, as their dormancy is alleviated by 4–8 weeks of stratification, enhancing sensitivity to light and temperature while maintaining hormonal regulation via the ABA-GA antagonism.[22]Deep PD imposes the strongest inhibition, necessitating extended cold periods (14 weeks to 15 months) for dormancy release, during which excised embryos either fail to grow or produce abnormal seedlings without stratification. GA typically has no effect on intact seeds at this level, reflecting profound insensitivity to germination cues. This subtype is common in temperate forest herbs and trees, such as Norway maple (Acer platanoides), where long stratification synchronizes germination with stable spring conditions, and herbaceous perennials like hepatica (Hepatica nobilis), ensuring seedling establishment after prolonged winter exposure.[23] Across all levels, PD modulates seed banks' temporal dynamics, promoting population persistence in variable environments through regulated hormone signaling and cue responsiveness.[19]
Physical Dormancy
Physical dormancy (PY) is characterized by water impermeability of the seed or fruit coat, preventing imbibition and subsequent germination until the barrier is disrupted. This impermeability arises primarily from a palisade layer of lignified macrosclereids in the outer seed coat, often reinforced by hydrophobic substances such as cutin, suberin, and lignin that block water entry. PY is broken through scarification—mechanical abrasion—or environmental cues that trigger the opening of specialized structures known as water gaps, allowing water uptake.[24][21][25]The mechanisms of PY involve distinct water gap complexes, classified into types I through IV based on their anatomical structure and response to dormancy-breaking stimuli. For instance, Type I water gaps feature surface cell layers that separate under heat or chemical exposure, while Type II gaps involve hilar modifications that respond to abrasion or wetting-drying cycles; lignified macrosclereids in these regions maintain closure until environmental signals, such as fire-induced heat or microbial activity, cause them to fissure. These gaps are typically located at the hilum, micropyle, or strophiole, ensuring precise control over permeability. In legumes, the palisade layer's composition, including cutin-rich cuticles, further enhances impermeability by forming a hydrophobic barrier.[26][27][25]PY is prevalent in approximately 25% of angiosperm species globally, occurring in at least 18 families, with high incidence in Fabaceae (legumes) and Malvaceae. It is particularly common in species adapted to arid or fire-prone environments, where it promotes seed persistence in the soil seed bank. Representative examples include soybean (Glycine max), where "hard seeds" result from impermeable coats due to cutin and lignin deposition, requiring scarification for germination in agriculture. Similarly, fire-adapted Acaciaspecies exhibit heat-sensitive PY, with water gaps opening after exposure to temperatures around 80°C from wildfires, synchronizing germination with post-fire conditions.[28][25][29]Recent molecular research has elucidated the genetic regulation of PY in legumes, highlighting the role of cutin and lignin composition in seed coat impermeability. A 2024 review emphasizes that variations in cutin, composed of hydroxylated fatty acids, and lignin deposition in the palisade layer determine hardness, with environmental factors like temperature influencing their synthesis during seed maturation. Genes involved in fatty acid synthesis, such as KCS12 in Medicago truncatula (encoding a 3-ketoacyl-CoA synthase for very-long-chain fatty acids), regulate cuticle formation and permeability; mutants lacking this gene show reduced dormancy. In soybean, loci like GmHs1-1 (a calcineurin-like protein) and GmqHS1 (an endo-1,4-β-glucanase) control hard-seededness, with wild accessions displaying stronger PY than domesticated varieties due to altered fatty acid profiles. These advances underscore PY's genetic basis, aiding breeding for improved seed longevity.[25][30]
Morphological Dormancy
Morphological dormancy is a form of primary seed dormancy in which the embryo is rudimentary and underdeveloped at the time of seed dispersal, requiring post-dispersal growth and differentiation before germination can proceed. This developmental delay, caused by the embryo's incomplete maturation, typically lasts from several weeks to months, ensuring that germination does not occur immediately after dispersal. Unlike other dormancy types, MD involves no chemical inhibitors or physical barriers; the dormancy arises purely from the morphological immaturity of the embryo, which must elongate and develop organs such as cotyledons and the radicle.[31]A key characteristic of MD is the small size of the embryo relative to the seed, with the embryo length generally less than 50% of the seed length (embryo:seed length ratio < 0.5), indicating arrested development despite physiological competence. This condition is prevalent in specific angiosperm families, including Apiaceae (e.g., celery) and Papaveraceae, and is particularly common among herbaceous perennials in temperate regions, where it synchronizes germination with favorable seasonal conditions. Morphological dormancy is relatively rare compared to physiological or physical dormancy, representing a minority of primary dormancy cases across plant species.[32][31]Representative examples include species in the genus Trillium (Liliaceae), where seeds disperse in late summer with tiny embryos that grow slowly over winter under cool, moist conditions, enabling spring germination. Some orchid species (Orchidaceae) exhibit MD with even prolonged delays, as their minute "dust seeds" feature highly underdeveloped embryos that may take months to mature, often extending beyond typical timelines due to the embryo's extreme smallness.[33][31]Breaking morphological dormancy primarily involves warm stratification, which stimulates embryo elongation and completion of development, typically without the need for cold exposure or specific light requirements. In cases where MD co-occurs with physiological dormancy, the result is morphophysiological dormancy, requiring additional cues to fully release germination potential.[31]
Morphophysiological Dormancy
Morphophysiological dormancy (MPD) is a complex form of primary seed dormancy characterized by the presence of both morphological and physiological dormancy components in the seed at maturity. The morphological component involves an underdeveloped embryo that is less than 50% the length of the seed and requires time for growth to reach a critical size sufficient for germination. Simultaneously, the physiological component imposes an innate inhibition on germination, even after the embryo has matured, necessitating specific environmental cues to alleviate the dormancy. This dual requirement ensures that germination is delayed until conditions are optimal, often synchronizing with seasonal changes in temperate environments.MPD is classified into subtypes based on the timing of embryo growth relative to the breaking of physiological dormancy and the depth of the physiological component. Simple MPD occurs when embryo elongation and the alleviation of physiological dormancy happen under the same temperature regime, typically requiring a single cue sequence. In contrast, complex MPD involves distinct phases, where embryo growth and dormancy release occur separately, often demanding multiple environmental cycles. The physiological aspect further divides into nondeep (broken by relatively short cold stratification of 4-8 weeks at 5°C), intermediate (requiring warm followed by cold stratification), and deep (needing prolonged cold exposure of 8-16 weeks or more). Recent revisions to the Nikolaeva-Baskin system have expanded MPD into 12 subclasses, 24 levels, and 16 types to account for variations in epicotyl dormancy and cue sequences, enhancing precision in ecological studies.[8][12]This dormancy type is prevalent among seed plants, accounting for approximately 18% of species with primary dormancy in global databases, and is especially common in perennial herbs of temperate woodlands. The family Ranunculaceae shows a particularly high incidence, with many species exhibiting MPD to align germination with spring conditions after winter. Examples include Delphinium tricorne, which demonstrates deep complex MPD requiring sequential warm and cold stratification for embryo maturation and dormancy release. In alpine contexts, variations in intermediate complex MPD have been documented in Aconitum barbatum, where maternal environment and after-ripening influence the degree of dormancy, as shown in 2023 studies highlighting adaptive flexibility in high-elevation Ranunculaceae.[10][35][36]Breaking MPD typically follows a specific sequence mirroring natural seasonal cycles: warm temperatures (15-25°C for 1-4 months) promote morphological embryo growth, followed by cold stratification (5°C for 2-6 months) to overcome the physiological block, with germination often occurring in subsequent warm conditions. The total time required in nature can span 1 to 5 years, depending on the subtype and environmental variability, ensuring seedling establishment avoids unfavorable periods like summer drought or early frost. Unlike pure morphological dormancy, which relies solely on time for embryo development without additional physiological cues, MPD's integrated barriers provide finer temporal control over germination timing.[8][37]
Combinational Dormancy
Combinational dormancy, classified as PY + PD in the standard seed dormancy system, occurs when seeds possess both a water-impermeable layer in the seed or fruit coat (physical dormancy, PY) and physiological inhibition of the embryo (physiological dormancy, PD). This dual mechanism ensures that germination is prevented until both barriers are sequentially overcome, providing a robust adaptation to environments where premature germination could be fatal. The impermeable coat blocks water entry, while the dormant embryo remains unresponsive even if water were available, often due to hormonal imbalances such as elevated abscisic acid (ABA) levels.[8][21]This form of dormancy is phylogenetically derived and relatively rare, documented in fewer than 5% of angiosperm species worldwide, though it is notably prevalent in specific families like Geraniaceae and certain legumes in Fabaceae. For instance, seeds of Geranium robertianum exhibit combinational dormancy where the physical barrier is lost during summer exposure to high temperatures or fire cues that crack the seed coat, followed by physiological release triggered by light or after-ripening in autumn, ensuring seedling emergence aligns with favorable moist conditions. Similarly, Rhus aromatica (Anacardiaceae) requires initial scarification to break PY before PD can be alleviated, highlighting how this dormancy type synchronizes germination with seasonal environmental shifts in fire-prone or variable habitats.[20][38][21]Breaking combinational dormancy demands a two-step process: first, physical treatments like mechanical or chemical scarification, dry heat, or fire to permeabilize the coat, followed by physiological alleviation via cold stratification, gibberellin (GA) application, or extended after-ripening to reduce ABA sensitivity in the embryo. Recent studies have begun elucidating the molecular underpinnings, revealing interactions between seed coat structural genes (e.g., those regulating permeability via lignin deposition) and ABA biosynthetic pathways that maintain PD until the coat is breached, allowing GA signaling to promote embryo expansion. This sequential nature poses challenges for ecological restoration, where mimicking natural cues—such as prescribed burns followed by moist chilling—is essential to achieve viable germination rates in species like Geranium for habitat rehabilitation.[21][39]
Secondary Dormancy
Definition and Induction
Secondary dormancy is defined as the imposition of a dormant state on imbibed, viable seeds that were previously non-dormant and capable of germinating under favorable conditions, typically triggered by exposure to adverse environmental factors. This dormancy is reversible, with germination resuming once conditions return to suitability, thereby serving as an adaptive mechanism to avoid germination during transient unfavorable periods.[40]Unlike primary dormancy, which is an inherent trait established during seed maturation on the parent plant and present at the time of dispersal, secondary dormancy develops post-dispersal in response to external stresses encountered by mature seeds.[41] Seeds that have lost primary dormancy, such as physiological or physical dormancy, can enter secondary dormancy after initial release.[8]Induction of secondary dormancy involves specific environmental cues that impose dormancy on germinable seeds, including thermodormancy—caused by exposure to high or low temperatures that inhibit germination despite prior capability—or photodormancy, induced by prolonged light or darkness periods that alter sensitivity to germination stimuli. Chemical stresses, such as hypoxia (oxygen deficiency) or exposure to certain inhibitors, can also trigger induction by disrupting metabolic processes necessary for germination.[40][42][43][44]This phenomenon is particularly prevalent in weed species within crop fields and arable soils, where it enhances the longevity of soil seed banks by enabling seeds to persist without germinating during suboptimal seasons, thus contributing to weed population dynamics and management challenges. It also plays a role in crop seeds, aiding persistence in seed banks and influencing traits like pre-harvest sprouting resistance in cereals.[45][46][47]Secondary dormancy serves as a dynamic extension of physiological dormancy, allowing seeds to cycle between dormant and non-dormant states in response to fluctuating environmental conditions.
Environmental Triggers
Secondary dormancy in seeds is induced by various environmental factors that signal unfavorable conditions for germination, preventing radicle emergence and promoting survival until conditions improve. These triggers act on imbibed, non-dormant seeds, shifting them into a dormant state through physiological adjustments. Abiotic factors such as temperature, light, water availability, and oxygen levels are primary inducers, while biotic interactions from surrounding organisms can also contribute.[48][49]Temperature plays a critical role in inducing secondary dormancy, particularly through supra-optimal or sub-optimal ranges that inhibit germination processes. In cereals like barley, exposure to temperatures above 30°C during imbibition triggers thermodormancy, preventing radicle protrusion even after return to permissive conditions, as seen in grains incubated at 30°C for 1–3 days. Low temperatures can prolong dormancy or induce secondary dormancy in some cereals, simulating cold stress that maintains dormancy potential under prolonged chilling. These temperature cues often lead to hormonal shifts, such as increased abscisic acid levels, reinforcing the dormant state.[50][47]Light quality and photoperiod significantly influence secondary dormancy, especially in species sensitive to burial or seasonal light changes. Extended long-day regimes, such as 16 hours of light followed by 8 hours of darkness, induce secondary dormancy in seeds of the Mediterranean plant Aethionema arabicum, repressing germination to align with cooler seasons and reducing it to near 0% after 7 days of exposure. In light-requiring species like common ragweed (Ambrosia artemisiifolia), prolonged darkness promotes entry into secondary dormancy by late spring, inhibiting germination across temperature ranges in both light and dark conditions.[51][52]Water and oxygen availability are key abiotic triggers, with deficits or excesses signaling environmental stress. Hypoxia, often from flooded soils, induces secondary dormancy in imbibed seeds by limiting oxygen diffusion, as observed in barley and other cereals where low oxygen tensions prevent germination and activate dormancy pathways via the N-degron system. Desiccationstress, through low water potentials in drying soils, similarly imposes secondary dormancy in weed seeds like Scotch thistle (Onopordum acanthium), where cycles of wetting and drying enhance dormancy depth to avoid germination during drought.[53][54][55]Biotic factors from neighboring plants and soil microbes contribute to secondary dormancy induction via chemical signaling. Allelochemicals released by competing plants, such as phenolic compounds, inhibit seed germination and maintain dormancy by disrupting hormonal balance and membrane permeability in target seeds. Microbial signals, including volatile compounds from soilbacteria, can modulate dormancy in the seed microbiome, influencing germination inhibition under biotic stress conditions.[56][57][58]Recent research highlights the integration of these triggers at the molecular level; for instance, a 2024 study on wheat seeds demonstrated that heat exposure at 38°C during early imbibition induces secondary dormancy, with non-germinated seeds recovering viability upon transfer to 22°C, underscoring temperature's role in dormancy cycling.
Plant hormones play a central role in regulating both primary and secondary seed dormancy through intricate signaling pathways that control embryo growth and metabolic activity. Abscisic acid (ABA) is the primary promoter of dormancy, accumulating during seed maturation to inhibit germination by suppressing embryo expansion and maintaining metabolic quiescence.[59] In contrast, gibberellins (GA) counteract ABA effects by stimulating embryo growth and mobilizing storage reserves, thereby facilitating dormancy release and germination.[60]ABA achieves its dormancy-inducing function partly by inhibiting GA biosynthesis, creating an antagonistic interaction that fine-tunes seed responsiveness to environmental cues.[59]The balance between ABA and GA is pivotal, with dormant seeds exhibiting a high ABA/GA ratio that prevents germination.[60] During after-ripening, a dry storage process that alleviates primary dormancy, ABA levels decrease through enhanced catabolism, lowering the ABA/GA ratio and increasing seed sensitivity to germination signals.[60] In Arabidopsis thaliana, mutants such as ahg1-1 demonstrate ABA hypersensitivity, leading to deeper physiological dormancy due to exaggerated ABA signaling during seed imbibition.[61] Recent research highlights the role of 9-cis-epoxycarotenoid dioxygenase (NCED) genes in ABA biosynthesis; for instance, overexpression of SiNCED1 in foxtail millet elevates ABA content, enhancing seed dormancy and drought tolerance.[62] Similarly, PlNCED2 in Paeonia lactiflora promotes dormancy by boosting ABA accumulation in embryos.[63]Other hormones modulate dormancy in specific contexts. Ethylene breaks physical dormancy in species like cocklebur (Xanthium pennsylvanicum) by weakening impermeable seed coats and promoting radicle emergence, often at concentrations of 0.1–200 μL L⁻¹.[64] In morphophysiological dormancy, auxins maintain dormancy by stimulating ABA signaling through AUXIN RESPONSE FACTOR 10/16 (ARF10/16)-mediated activation of ABI3, while cytokinins counteract this by promoting embryo growth and cell division, as observed in Ferula assa-foetida seeds where cytokinin application enhances germination post-stratification.[65][66]Temperature shifts influence these hormonal interactions; for example, in sunflower seeds, a rise from 10°C to 20°C relocalizes ABA effectors like ABI5 to the cytoplasm, reducing ABA sensitivity and enabling dormancy release despite persistent ABA levels.[67] Genetic regulation upstream of hormone biosynthesis, such as through transcription factors like ABI4, further mediates the ABA-GA antagonism.[68]
Molecular and Genetic Factors
Seed dormancy is regulated at the molecular level by key genes that control the depth and timing of dormancy. In Arabidopsis thaliana, the DELAY OF GERMINATION 1 (DOG1) gene serves as a master regulator of primary dormancy, influencing the expression of genes involved in abscisic acid (ABA) and gibberellin (GA) metabolism to delay germination.[69] DOG1 protein levels directly correlate with dormancy strength, as seeds lacking functional DOG1 exhibit complete non-dormancy, and it interacts genetically with ABA signaling components to fine-tune dormancy responses.[70] Similarly, the ABI3 (ABSCISIC ACID INSENSITIVE 3) and VP1 (VIVIPAROUS 1) genes play central roles in ABA signaling during seed maturation and dormancy establishment; ABI3 acts as a transcription factor that promotes ABA sensitivity, while VP1 complements ABI3 function to restore ABA responsiveness in mutants, thereby enforcing dormancy.[39][71]Epigenetic mechanisms, including histone modifications and DNA methylation, provide dynamic regulation of dormancy, particularly in response to seasonal environmental cues. Histone marks such as H3K27me3, H3K9me, and H3K4me modulate the expression of dormancy-related genes like DOG1, enabling reversible control over seasonal dormancy cycles in response to temperature and light.[72]DNA methylation patterns, often concentrated in methylation valleys, repress or activate seed-specific genes to maintain dormancy states, with demethylation events facilitating transitions out of dormancy during favorable conditions.[73] These epigenetic layers allow plants to integrate environmental signals without altering the underlying DNA sequence, ensuring adaptive dormancy across generations.[74]Quantitative trait locus (QTL) mapping has identified genetic loci underlying physical dormancy (PY) in legumes, highlighting the role of seed coat genes in impermeability. In chickpea, QTLs on linkage groups LG1 and LG3 regulate seed coat development and filling, directly influencing PY by controlling permeability barriers.[25] A 2024 study on pea revealed that physical dormancy is genetically separable from other traits, with specific loci modulating seed coat thickness and composition to enforce dormancy.[75] These findings underscore how polygenic control in legumes evolves to adapt seed coats as primary barriers to water uptake.Transcription factors from the WRKY family further mediate dormancy release, particularly in secondary dormancy contexts. For instance, TgWRKY24 in Tulipa thianschanica responds to ABA signals to promote dormancy alleviation, binding to promoter regions of downstream targets to activate germination pathways.[76] This WRKY member exemplifies how transcription factors integrate hormonal cues to dynamically release dormancy under stress or after-ripening.From an evolutionary perspective, seed dormancy traits exhibit a polygenic architecture, with multiple loci contributing to variation in dormancy depth and contributing to trade-offs between rapid germination and enhanced survival in unpredictable environments.[77] Genetic correlations between dormancy, seed mass, and seedling vigor indicate that selection for dormancy often balances faster germination against improved persistence in seed banks, driving adaptive evolution in wild populations.[78] DOG1, for example, indirectly affects ABA levels to mediate these trade-offs.[69]
Breaking Seed Dormancy
Natural Breaking Processes
Natural breaking processes alleviate seed dormancy through environmental cues and physiological changes that occur in situ, enabling germination when conditions become favorable for seedling establishment. These mechanisms primarily target primary dormancy in freshly matured seeds or secondary dormancy induced in imbibed seeds under unfavorable conditions, ensuring timed release in natural ecosystems.[79]After-ripening involves the dry storage of seeds at ambient temperatures (typically 15-25°C), which gradually oxidizes germination inhibitors such as abscisic acid-derived compounds, thereby releasing non-deep physiological dormancy (PD). This process commonly requires 1-6 months and is widespread in families like Poaceae and Brassicaceae, where it promotes germination upon subsequent imbibition under suitable moisture and temperature.[80] During after-ripening, reactive oxygen species facilitate the degradation of dormancy-maintaining proteins, enhancing sensitivity to gibberellins that drive embryo growth.[81]Stratification exposes seeds to prolonged moist conditions at low temperatures (0-10°C) for cold variants or higher temperatures (15-25°C) for warm variants, effectively breaking morphophysiological dormancy (MPD) and deep PD by promoting embryo maturation and reducing inhibitor sensitivity. Cold stratification, lasting 3-12 months in many temperate species such as Apiaceae, mimics winter chilling to synchronize spring germination, while warm moist stratification suits subtropical taxa with MPD, often requiring sequential warm-then-cold phases for full alleviation.[79] These conditions trigger metabolic shifts, including decreased abscisic acid levels and increased gibberellin biosynthesis, which collectively overcome the physiological block.[82]For physical dormancy (PY), natural scarification occurs through mechanical abrasion by soil particles, microbial degradation, or passage through animal digestive tracts, which permeabilize the seed coat and allow water uptake. In pyrophyte species like those in Fabaceae and Rhamnaceae from fire-prone habitats, heat from wildfires cracks the water-impermeable palisade layer, releasing PY within hours to days post-fire and facilitating post-disturbance colonization.[83] Soil microbes, including fungi and bacteria, contribute by enzymatically weakening the coat over months to years, particularly in undisturbed litter layers.[84]Temperature cycling, involving diurnal or seasonal fluctuations (e.g., 10-30°C alternations), breaks secondary dormancy in imbibed seeds by simulating environmental variability, which induces rhythmic metabolic activation not achieved under constant temperatures. This process is crucial for weed and crop species in arable soils, where daily cycles over weeks promote germination flushes aligned with tillage or rainfall events.[85]
Artificial Alleviation Methods
Artificial alleviation methods encompass a range of human-intervened techniques designed to overcome seed dormancy barriers, facilitating controlled germination for agricultural, horticultural, and research purposes. These approaches mimic or enhance natural processes, such as afterripening or stratification, but apply them under precise conditions to accelerate outcomes.[86]Chemical treatments are among the most widely used for breaking physiological dormancy (PD), particularly through the application of gibberellic acid (GA3). Exogenous GA3 at concentrations of 100-500 ppm promotes embryo growth and enzyme activation in dormant seeds, effectively substituting for prolonged cold stratification in many species.[87] For light-sensitive seeds exhibiting PD, potassium nitrate (KNO3) solutions or smoke water extracts serve as effective stimulants; KNO3 at 0.2-2% enhances germination by modulating osmotic potential and nitrate signaling, while smoke water, derived from plant combustion, contains karrikins that trigger germination pathways similar to those activated by bushfires.[48]Physical methods target physical dormancy (PY) caused by impermeable seed coats, primarily through scarification. Acid scarification using sulfuric acid for 10-60 minutes, depending on species thickness, etches the coat to allow water imbibition, as commonly applied to legumes like Acacia and Trifolium.[86] Heat scarification, involving dry heat at 80-100°C for 5-30 minutes or hot water soaking, similarly permeabilizes coats in fire-prone species. Emerging precision techniques include ultrasound treatment, which uses sonic waves to create micro-fractures in the coat without chemical residues, achieving up to 80% germination improvement in hard-coated seeds, and laser biostimulation, where low-level lasers (e.g., He-Ne at 632.8 nm) alter coat permeability and metabolic activity.Hormonal antagonists address dormancy regulated by inhibitory hormones like abscisic acid (ABA). Fluridone, an ABAbiosynthesis inhibitor, applied at 1-10 μM, reduces ABA levels and promotes germination in species with deep PD, such as lettuce. Ethephon, an ethylene-releasing compound used at 100-1000 ppm, counters ABA inhibition by stimulating cell expansion and endosperm weakening, particularly effective in cereals and dicots.Advanced techniques leverage biotechnology and nanomaterials for targeted alleviation. Genetic editing via CRISPR/Cas9 targeting the DELAY OF GERMINATION 1 (DOG1) gene, a key dormancy regulator, has been used to create low-dormancy mutants in crops like Arabidopsis and wheat, reducing afterripening requirements by 50-70%. Recent advancements include nanotechnology, where nanoparticles such as carbon nanotubes or silver nanoparticles (at 10-100 mg/L) enhance coat penetration and hormone delivery, as reviewed in 2023 studies showing 20-40% germination boosts in dormant seeds without environmental harm.Practical examples illustrate these methods' efficacy. In walnuts exhibiting morphophysiological dormancy (MPD), combining GA3 (500 ppm) with 60-90 days of cold stratification at 4°C breaks dormancy, achieving 70-90% germination rates compared to 10% without treatment. For weed management, dormancy-breaking herbicides like those targeting ABA pathways induce germination in soil seedbanks, followed by tillage or herbicide application, reducing persistent populations by up to 60% in species like Avena fatua.
Applications and Implications
In Agriculture and Weed Control
In agriculture, seed dormancy plays a dual role in crop production by enabling uniform germination when strategically broken, particularly in hybrid varieties, which enhances stand establishment and yield consistency. Breaking dormancy through methods like after-ripening or chemical treatments allows hybrid seeds to synchronize emergence, reducing variability in field planting and improving overall crop performance. For instance, in wheat, maintaining appropriate dormancy levels via abscisic acid (ABA)-related mechanisms prevents pre-harvest sprouting, a condition where grains germinate prematurely on the plant, leading to quality degradation; ABA-insensitive mutants have been identified that reduce dormancy and increase sprouting susceptibility, underscoring the value of balanced dormancy in breeding programs.[88][89]However, excessive dormancy in hybrid seeds poses challenges, such as delayed or uneven germination that can postpone planting timelines and lower yields in time-sensitive cropping systems. Marker-assisted selection (MAS) for dormancy-related traits has enabled breeders to incorporate quantitative trait loci (QTLs) that fine-tune dormancy levels, facilitating faster hybrid establishment without compromising other agronomic qualities. Recent studies (2024-2025) have identified major QTLs for pre-harvest sprouting resistance in crops like wheat and cucumber, supporting targeted breeding.[90][91] In rice, issues with incomplete or "false" dormancy—where seeds appear dormant but exhibit erratic germination—complicate hybrid production and contribute to inconsistent stands, necessitating targeted breeding to mitigate these effects. A 2025 study on molecular regulation of rice seed dormancy highlights advances in understanding these mechanisms for improved synchronization.[92][6]Seed dormancy is also leveraged in weed control strategies, where secondary dormancy is exploited to deplete persistent soil seedbanks through induced germination followed by tillage or herbicide application. Stimulants such as karrikinolide, a smoke-derived compound, trigger "suicidal germination" in dormant weed seeds, prompting them to sprout out of sync with crops and enabling their elimination before establishment. For example, in sorghum fields, shattering seeds from wild relatives like shattercane form long-lived seedbanks due to innate dormancy, persisting for years and reinfesting crops; management exploits this by promoting germination to reduce bank viability over time. Breeding efforts focus on adjustable dormancy in crops to counter such weeds while maintaining productivity.[93][94][95]Dormancy-related issues, particularly pre-harvest sprouting, contribute to economic losses in grain crops estimated at 10-20% of potential yield in susceptible varieties, driven by reduced grain quality and market value. These impacts highlight the importance of breeding for tunable dormancy to balance harvest reliability with field establishment.[96][97]
Seed banks play a pivotal role in conservation by leveraging the inherent dormancy of seeds to facilitate long-term ex situ storage, preserving genetic diversity for potential reintroduction into degraded habitats. The Svalbard Global Seed Vault, for instance, maintains duplicates of global crop and wild species collections under controlled cold and dry conditions that mimic and extend natural dormancy states, allowing seeds to remain viable for decades or even centuries.[98] This approach hedges against biodiversity loss from habitat destruction or environmental catastrophes, with dormancy acting as a natural buffer that the vault's permafrost environment amplifies.[99]For reintroduction efforts targeting endangered species, controlled breaking of seed dormancy is crucial to synchronize germination with favorable field conditions and enhance establishment success. Techniques such as mechanical scarification, acid etching, or thermal treatments are commonly applied to overcome physical or physiological barriers, as demonstrated in protocols for rare plants like Iliamna corei, where dry-heating and boiling water dips achieved high germination rates.[100] Similarly, for species exhibiting morphophysiological dormancy, such as exceptional endemics, combined warm and cold stratification pretreatments alleviate embryo immaturity and physiological inhibition, supporting propagation for habitat restoration.[101] These methods ensure that stored seeds from gene banks can be effectively deployed to bolster populations of threatened flora.Climate change poses significant risks to seed dormancy dynamics by shifting environmental cues, such as reduced chilling from warmer winters, which can desynchronize germination timing and lead to seedling mortality in mismatched seasons. In temperate and alpine regions, shorter cold stratification periods disrupt the release of physiological dormancy, potentially causing seeds to germinate prematurely or fail to germinate altogether, as observed in snowbed species where warming altered germination responses to temperature.[102] Recent analyses indicate that these disruptions may contribute to habitat homogenization and place substantial portions of plant species at risk, with models projecting heightened vulnerability for those reliant on specific seasonal cues.[103] For instance, in alpine ecosystems, species with morphophysiological dormancy (MPD) are particularly susceptible, as elevated temperatures during seed development and dispersal reduce the efficacy of required cold periods for embryo growth and germination.[104]Adaptation strategies in conservation emphasize selecting genotypes with flexible dormancy traits during restoration projects to better cope with variable climates, prioritizing sources from edges of species ranges that exhibit broader germination tolerances. In ecological restoration, this involves screening for seeds that respond adaptively to altered stratification needs, as seen in wetland initiatives where dormancy-breaking protocols like cold stratification and scarification are tailored to enhance establishment under projected warming scenarios.[105] Such approaches mitigate risks for vulnerable MPD taxa in alpines by incorporating assisted migration or trait-based sourcing to align dormancy release with shifting seasonal windows.[106]Illustrative examples highlight dormancy's conservation challenges amid global change. In Australian fire-prone ecosystems, species with physical dormancy (PY), such as many Fabaceae, depend on heat from wildfires to scarify impermeable seed coats and trigger germination; however, altered fire regimes—more frequent or intense due to climate-driven drought—threaten recruitment by exhausting soil seed banks before cues align, endangering PY-adapted endemics.[107] PY release in these contexts integrates thermal thresholds, but regime shifts disrupt this pyro-thermal niche, reducing post-fire seedling densities.[108] In peatland conservation, dormancy assays evaluate physiological dormancy prevalence—observed in nearly 90% of tested species—and guide alleviation via dry after-ripening or gibberellic acid treatments, enabling targeted sowing to restore degraded bogs and maintain hydrological functions.[109]A 2021 study on breaking hard seed dormancy in the perennial legume Lebeckia ambigua demonstrated effective methods like heat exposure to reduce impermeability, supporting propagation for conservation and sustainable agriculture. These techniques, informed by seed coat permeability studies, enhance germination for hard-seeded legumes vulnerable to habitat loss, integrating into broader strategies for resilient conservation networks, as highlighted in a 2025 analysis of physical dormancy in intensified farming systems.[110][111][112]