When should a seed germinate? This question can decide the fate of a plant species. During evolution, species adapted to their surroundings and regulatory mechanisms emerged to ensure germination when the environment is favorable. These environmental monitoring mechanisms and decision responses collectively regulate germination timing through seed dormancy. Domestication interferes with this natural postponing mechanism as it aims for fast and uniform germination. The resultant accelerated germination in modern crop varieties results in reduced or complete lack of seed dormancy, inadvertently increasing susceptibility to pre-harvest sprouting (PHS), a phenomenon in which seeds germinate on the mother plant before harvest (Gubler et al., 2005). With climate change causing erratic rainfall during harvest seasons, PHS is becoming a substantial problem and leading to worldwide yield loss (Black et al., 2006). An effective solution could be to retrieve (part) of the original plant strategies, ideally a very strong, but quickly removable dormancy at maturity. To achieve this goal, a thorough understanding of seed dormancy and germination is indispensable.

Germination is defined as the sequence of physiological events that initiate with water uptake (imbibition) by the dry seed and conclude with radicle protrusion through the seed coverings (Bewley, 1997). If environmental conditions required for germination, such as ample moisture, optimum temperature, and oxygen, are not met, the seed does not germinate. This can be referred to as lack of germination rather than the presence of dormancy. These seeds can resume germination as the environment becomes favorable (Baskin and Baskin, 2004). In contrast, “seed dormancy refers to the inability of a viable seed to germinate even under otherwise favorable environmental conditions, due to an internal block” (Finch-Savage and Leubner-Metzger, 2006; Karssen et al., 1983). While the release of dormancy is affected by environmental signals, the genetic background of the plant controls the depth, rate of dormancy loss, and nature of environmental cues required to break dormancy. Thus, dormancy reflects a genetically programmed and environmentally modulated endogenous mechanism (Considine and Considine, 2016).

Dormancy enables seeds to monitor seasonal and temporal cues, assess competition, and sense nutrient availability, thereby ensuring the optimal timing to germinate. Furthermore, dormancy acts as a bet-hedging strategy to spread out germination timing, distance from mother plant, and maximize survival (Thompson and Ooi, 2010). Experimentally, seed dormancy levels can be evaluated through a germination test. Parameters like final germination percentage or time-integrated matrices, such as germination index, are commonly used (Strand, 1980). This is why experiments need to be carefully designed and interpreted to distinguish the two processes. In the laboratory, primary seed dormancy can be assessed using freshly harvested seeds, while seed germination can be tested using after-ripened (non-dormant) seeds (Bethke et al., 2004).

Though seed dormancy can be categorized in different ways, five major classes have been distinguished and widely utilized, namely morphological, physiological, physical, morphophysiological, and combinational dormancy (Baskin and Baskin, 2004). In physiological dormancy, mature seeds stay dormant by internal physiological and metabolic restrictions within the embryo, so-called embryo-imposed dormancy, rather than the seed coat or underdeveloped seed structures. In temperate cereals and Arabidopsis, only physiological dormancy is relevant, which constitutes the focus of this manuscript (Bewley, 1997). Physical dormancy is caused by one or more water-impermeable layers of palisade cells in the seed or fruit coat (Baskin and Baskin, 2004). Although seed coverings and seed coat in temperate cereals can influence germination by interfering with gas exchange, namely coat-imposed dormancy, they do not cause true physical dormancy (Simpson, 1990).

Based on the timing of dormancy induction, it can be primary or secondary. Primary dormancy is established within the mother plant during seed development (Karssen et al., 1983). At physiological maturity, seed dormancy levels may range from deeply dormant to fully nondormant (Bewley, 1997). After dispersal, primary dormancy can be lost gradually, but afterwards, seeds may acquire secondary dormancy if they experience long-term unfavorable environmental conditions, such as hypoxia or extreme temperatures. Notably, secondary dormancy can only be induced with some residual primary dormancy, emphasizing the hierarchical relationship (Baskin and Baskin, 2004).

Studying seed dormancy in cultivated cereals is not always straightforward, mainly due to the absence of natural variation because of long-term artificial selection for reduced dormancy (Tai et al., 2021). The complex genomes of cereal crops make it even harder to tap into these genetic resources. Furthermore, cereals are often recalcitrant to genetic transformation, hindering the effective application of available functional genomic tools (Chen et al., 2022). Using a closely related “crop model” with similar growth conditions can accelerate research on this trait. Oryza sativa (rice) could be a practical option for investigating seed dormancy in tropical cereals, but it is not ideal for temperate cereals due to different growth conditions (Fujino et al., 2004). A model system like Brachypodium distachyon carries unique opportunities with abundant resources and tools (Mur et al., 2011). Although research on seed dormancy in Brachypodium is still in its infancy, previous discoveries in Arabidopsis can be a good starting point for translation to temperate grasses (Scholthof et al., 2018).

Arabidopsis thaliana has been instrumental in advancing our understanding of plant developmental mechanisms, including seed dormancy. Extensive research on this model organism has elucidated the genetic and environmental regulation of dormancy by factors such as light, nitrogen, temperature, and phytohormones (Bethke et al., 2006; Footitt et al., 2013; Hilhorst and Karssen, 1988). These studies provided important insights into dormancy mechanisms, such as major ABA and GA metabolism genes, hormonal signaling pathways and key dormancy regulators like DELAY OF GERMINATION 1 (DOG1) (Sajeev et al., 2024). However, due to evolutionary diversification in morphology, physiology and ecology, translating findings from Arabidopsis to the economically important temperate cereals faces multifaceted challenges (Roeder et al., 2025; Uauy et al., 2025).

In this review, we provide a comparative overview of dormancy and germination regulation between Arabidopsis and representative temperate cereals. These include the conserved central hormone balance between ABA and GA, the key player DOG1, and environmental regulation of seed dormancy induction and release, while also bringing up recent progress in epigenetic regulation of seed dormancy and PHS resistance. By highlighting shared and species-specific genetic pathways, we aim to elucidate areas that can be adapted from existing knowledge, while also pointing out gaps and opportunities that warrant further investigations. As such, we explore the potential use of these genetic pathways in addressing the problem of pre-harvest sprouting.

As an emerging problem, PHS stems from a lack of grain dormancy and is under strong environmental influence, most notably rainfall, temperature, and humidity (Tai et al., 2021). PHS induces precocious seed germination by shifting the hormonal balance, resulting in cellular and oxidative damage, reduced desiccation tolerance and increased susceptibility to pathogens, hence affecting seed viability (Black et al., 2006; Espinosa-Ramírez et al., 2021). During harvest season, sprouting on the mother plant initiates embryo-driven reserves mobilization through enzymes like α-amylase and proteases, leading to starch and protein breakdown in the endosperm (Matilla, 2024). In wheat, elevated α-amylase activity caused by PHS degrades starch into smaller sugars, lowering the Hagberg falling number, which is a measure of α-amylase activity through dough viscosity (a low falling number means high enzyme activity). This results in dense and gummy bread textures, rendering the grain unsuitable for baking. Partial sprouting, though not visible, can still lead to similar enzymatic effects. Furthermore, reduced viability disqualifies the grain from being used as a seed. Consequently, PHS-affected wheat is typically relegated to feed quality (Olaerts and Courtin, 2018). Barley, bred for uniform and early germination for malting, faces even more severe challenges because even mild PHS can drastically reduce grain quality. Partial cell wall breakdown during malting also increases β-glucan levels, leading to cloudy beer and industrial filter clogging. Like wheat, barley also suffers yield losses, and high moisture in sprouted seeds elevates the risk of fungal infection (Rooney et al., 2023).

Maintaining a manageable level of dormancy in commercial cereals offers a potential solution to PHS. A controllable switch from dormancy to germination, such as time-based after-ripening, is highly desirable (Rodríguez et al., 2015). A different “switch” in the form of a low-cost chemical or environmental treatment to trigger quick dormancy release could also be useful. While agronomic practices, like induced drought and variable nitrogen dosing, have been reported to be effective in enhancing PHS resistance, breeding for moderate dormancy remains the most sustainable approach for resistance (Biddulph et al., 2005; Yang et al., 2025b). The optimal dormancy level varies based on cereal species and end-use. In wheat used for baking, deep dormancy does not hinder industrial use, though it interferes with use as seed. For bread wheat intended for seed, moderate dormancy at physiological maturity, requiring 4–6 weeks of after-ripening, is ideal. Conversely, for industrial malting barley, very low dormancy is essential. Maltsters require high germination rates and speed, as any residual dormancy raises operational costs. The ideal dormancy pattern for barley should resist PHS while being malting-compatible, with a short after-ripening period (1–2 weeks) and uniform germination capability (Woonton et al., 2005). Other cereals, such as oats and rye, generally exhibit stronger dormancy (Simpson, 1990). Overall, similar principles apply that low dormancy or rapid dormancy loss is needed for germination based industrial processing, while uniform field germination is crucial for seeding establishment in agriculture. Thus, a relatively high dormancy with a quick controllable loss of dormancy would be ideal for commercial cereals (Figure 1).

To achieve this ideal dormancy pattern, the temperate grass model plant Brachypodium distachyon (purple false brome) offers unique advantages. It has a small diploid genome (~300 Mb), a short life cycle, and close physiological resemblance to temperate grasses. Moreover, it is self-pollinated, short-statured, and easily transformable, making it ideal for functional studies (Alves et al., 2009; Brkljacic et al., 2011). For seed dormancy and germination study, Brachypodium, as an undomesticated wild grass, could be superior to commercial varieties, owing to its extensive variation in seed dormancy and germination timing (Barrero et al., 2012; Kosina and Tomaszewska, 2016). Anatomical studies indicate a shared spikelet style of floral structure between Brachypodium and temperate cereals (Barrero et al., 2012; Opanowicz et al., 2008). Furthermore, Brachypodium seeds respond to dormancy-imposing and dormancy-breaking environmental conditions like temperate cereals. The effect of maternal temperature, light and after-ripening on Brachypodium seed dormancy has been characterized, showing consistent behaviors across grass species (Barrero et al., 2014, 2012; Elgabra et al., 2019; Li et al., 2019; Vidaller et al., 2018). Finally, Brachypodium grains contain most cell wall polysaccharides found in other cereal grains (Guillon et al., 2011; Hands and Drea, 2012). The roles of husks and membranes, anatomical observations of coleorhiza and embryo behavior during the early stages of grain germination have been extensively explored by independent research (Barrero et al., 2012; El-Keblawy et al., 2019; Wolny et al., 2018). Notably, endo-beta-mannanase and cathepsin B-like protease, known influencers of Arabidopsis and tomato seed germination, have been shown to play similar roles during wheat, barley and Brachypodium grain germination (Gonzalez-Calle et al., 2015; Iglesias-Fernández et al., 2019; Isabel-LaMoneda et al., 2003). In addition, epigenetic modifications have also been examined during Brachypodium grain germination, which may provide resources to develop comparable insights when integrated with data from wheat and barley (Gao et al., 2012; Kapazoglou et al., 2010; Wolny et al., 2017). Given its physiological similarity to temperate cereals and genetic tractability, Brachypodium distachyon holds the potential of a powerful model for seed dormancy research, which could accelerate the discovery of functional genes and their regulatory mechanisms, ultimately aiding breeding efforts for PHS resistance in wheat, barley, and other temperate cereals. However, more intensive investigation would be anticipated to deepen our understanding of seed dormancy and germination regulation and assist knowledge translation into economically important temperate cereals.

Seed morphology is an important factor in the regulation of seed dormancy. A typical desiccation-tolerant or orthodox seed consists of a combination of living and dead tissues. Dead tissues mainly contribute to physically preventing the seed from germinating through specialized structures and hardened seed coats or seed coverings. They can influence germination by interrupting water or oxygen uptake or by physically blocking the embryo from emerging. In addition, certain molecules present in the testa or husk can regulate dormancy.

In Arabidopsis seeds, the ovule integuments form the dead testa (seed coat), but unlike cereals, they lack a husk (Table 1). During seed maturation, the outer layer accumulates a waxy cuticle, while the inner membrane develops different pigments such as flavonoids (proanthocyanidins) and tannins (Figure 2A). The presence of these pigments creates a tight hydrophobic layer that affects oxygen and water uptake during imbibition. Additionally, Arabidopsis seed coats accumulate the fatty polymer suberin, which also interferes with oxygen exchange (Fedi et al., 2017). Considering the involvement of protein and mRNA oxidation in after-ripening and germination, the link between these processes and the seed barrier has been extensively characterized (El-Maarouf-Bouteau et al., 2013). Experimentally, water uptake is tested using dyes such as tetrazolium. In non-dormant seeds with more permeable testa, higher water uptake was observed. Scarification (physical damage to the seed coat) can increase germination in deeply dormant seeds. Consistent with this, Arabidopsis transparent-testa (tt) mutants—tt2 (encoding an R2R3 MYB domain protein), tt4 (encoding chalcone synthase), and ttg1 (encoding a WD-repeat-containing protein)—produce seeds lacking proanthocyanidins and germinate faster than wild-type controls (Debeaujon et al., 2000). Moreover, suberin and flavanols have been found to modify seed coat structure through temperature-dependent lignification (Hyvärinen et al., 2025; MacGregor et al., 2015). Low temperature during mother plant development promotes lignification and suberization of a polar lignin barrier in the outer integument cells of seeds. Transcription factors MYB9 and MYB107 were confirmed to be responsible for these modifications, with predominant contribution from MYB107 under cold temperature and a lesser role played by MYB9 (Hyvärinen et al., 2025).

Besides seed coats, Arabidopsis endosperm contributes to seed dormancy significantly, though it is very small in size compared to embryos and does not contain major storage compounds (Bethke et al., 2007). However, the single-celled aleurone-like-layered endosperm plays crucial roles in regulating seed dormancy through phytohormone signaling. The Arabidopsis endosperm maintains dormancy by providing ABA-rich hormonal suppression, restricting GA signaling, resisting radicle emergence, and modulating embryo growth through maternal and gene-regulatory signals (Doll and Ingram, 2022). During seed development, the endosperm-expressed transcription factors ZHOUPI and INDUCER OF CBF EXPRESSION 1 determine the depth of primary seed dormancy in Arabidopsis (MacGregor et al., 2019). Upon seed imbibition, endosperm responds to nitric oxide, GA and ABA. ABI5 expression in the endosperm defines altered and spatially distinct ABA signaling in contrast to ABI4 expression confined to the embryo (Penfield et al., 2006b). In addition, endosperm controls seed germination via mannanase mediated radicle emergence and release or transport of ABA into the embryo (Iglesias-Fernández et al., 2011; Kang et al., 2015; Lee et al., 2010; Leubner-Metzger, 2002).

The cereal grain (caryopsis) has a thin testa fused to the pericarp. The lemma and palea (collectively called the husk) enclose the seed, either loosely (e.g., wheat) or tightly (e.g., barley, Brachypodium). In cereals, the seeds are relatively large with a single cotyledon (Figure 2B). The combined outer coverings (testa and husk) play a major role in coat-imposed dormancy, similar to Arabidopsis. These structures accumulate various phenolic compounds, including phenolic acids, coumarins, tannins, and flavonoids. Many of these compounds have been shown to strongly inhibit germination (Rusu et al., 2023). One important chemical group is the flavan-4-ols, precursors of phlobaphenes responsible for red coat color in wheat, barley, and rice (Groos et al., 2002; Himi et al., 2005). Notably, the wheat R-1 locus (also called PHS-3D) encodes a MYB-type transcription factor named Tamyb10, which controls husk and coat pigmentation (Himi and Noda, 2005; Lang et al., 2021). Overexpression of Tamyb10-D in the white-grained wheat cultivar Fielder led to red-grained seeds showing significantly delayed germination, which correlated with higher flavonoid and ABA production contributed by upregulated expression level of genes in the flavonoid biosynthesis pathway and ABA biosynthesis pathway (Lang et al., 2021). In rice, the RED COLEOPTILE LOCUS (OsRc) controls seed dormancy and pigmentation by regulating ABA and flavonoid biosynthetic pathways, respectively (Gu et al., 2011). Phylogenetic analysis revealed high sequence similarity between OsRc, Tamyb10, the barley proanthocyanidin synthesis locus (Ant28; candidate gene HvMYB10), and the Arabidopsis TRANSPARENT TESTA (TT) genes (Furukawa et al., 2007).

In temperate cereals, husks can hinder oxygen uptake and enhance dormancy; their removal may therefore reduce dormancy (Barrero et al., 2012; Bradford et al., 2008). Although the husk remains tightly attached in barley, it plays a particularly significant role. It has also been suggested that the husk functions as a light filter, allowing only certain wavelengths to pass and thus affecting germination. At least in wheat, water movement did not differ significantly between dormant and non-dormant seeds, ruling out reduced water availability as the main reason for husk-imposed dormancy (Rathjen et al., 2009). Instead, oxygen uptake is the key factor, as shown by the fact that dormant barley seeds can germinate more readily in a high-oxygen environment (Bradford et al., 2008). Phenolic compounds in the husk likely serve as substrates for oxidation reactions, creating a low-oxygen atmosphere and reducing respiration in the aleurone layer and embryo. Oxygen uptake in temperate cereals is also temperature-regulated: under 15 °C incubation, oxygen content beneath the husk may rise to 15.8%, whereas at 30 °C it can drop to 0.3% (Hoang et al., 2014). After-ripened grains show a reduced effect of husk-imposed dormancy, even though they do not exhibit significant differences in phenolic compound composition (Rodríguez et al., 2015).

Endosperm in cereals is a large persistent tissue and contains major storage molecules with a surrounding aleurone layer. The large endosperm occupies most of the grain volume (Barrero et al., 2012; Kesavan et al., 2013). At maturity, the endosperm is mostly starchy and functions as a dead storage tissue, with a living single-celled aleurone layer (Liang et al., 2025). Unlike Arabidopsis, which consumes most of its endosperm during embryogenesis, cereals retain the endosperm as the primary storage tissue. The aleurone layer acts as a major regulator of dormancy by maintaining high ABA sensitivity and upregulating the ABA responsiveness genes in dormant seeds, while also functions as a signaling component for the embryo (Matilla, 2024). Moreover, cell wall modification and α-amylase activation occur through the aleurone layer (Hedden, 2025).

Additionally, studies in grasses, including barley, Brachypodium and oat, have shown that the coleorhiza tissue plays a pivotal role in causing dormancy and preventing germination, mainly through inhibiting ABA catabolism and affecting cell wall modification (Barrero et al., 2009; Gonzalez-Calle et al., 2015; Holloway et al., 2021; Millar et al., 2006). Coleorhiza hairs developed on rice embryo surfaces have also been implicated in grain germination, but through a distinct mechanism related to atmospheric moisture uptake (Bin Rahman et al., 2022).

Overall, seed covering structures can play a major role in both temperate cereals and Arabidopsis for dormancy regulation, although the influence is generally more prominent in cereals due to the presence of husks. With respect to PHS, dormancy regulation through the husk is particularly relevant. Coat/husk-imposed dormancy interacts with embryo-regulated dormancy to determine the final dormancy level. Later sections will discuss embryo-regulated dormancy in more detail.

DELAY OF GERMINATION 1 (DOG1) was initially identified as a quantitative trait locus (QTL) for natural variation of dormancy in Arabidopsis (Bentsink et al., 2006). It encodes a protein that lacks domains with a known function. However, more recent studies revealed DOG1 is an α-helical protein that binds heme and interacts with ABA‐related PP2C phosphatases (Nishimura et al., 2018). In Arabidopsis, AtDOG1 regulates dormancy induction, release, depth and dormancy cycling (Dekkers and Bentsink, 2015). It shows seed-specific expression and peaks at the late maturation stage (Bentsink et al., 2006). Inter-accession AtDOG1 expression variation has been associated with seed maturation environment, while its transcript and protein levels positively correlate with seed dormancy levels in a temperature-dependent manner (Chiang et al., 2011; Nakabayashi et al., 2012). AtDOG1 transcripts remain present in after-ripened seeds and disappear rapidly in both after-ripened and dormant seeds upon imbibition. Its protein localizes to the nucleus, and its abundance in freshly harvested seeds is highly correlated with the depth of dormancy. However, this correlation disappeared during after-ripening, which may be explained by possible protein modification, loss of self-binding or heme binding capacity (Nakabayashi et al., 2015, 2012; Nishimura et al., 2018).

As a central regulator of seed dormancy, ABA strongly influences the role of DOG1 in seed dormancy. Connections between AtDOG1 and ABA have been revealed at both the genetic and protein levels. The dog1 loss-of-function mutant seeds show complete germination without after-ripening requirement and retain normal ABA sensitivity, while combination of dog1 with GA biosynthesis mutant ga1–3 or imbibition with GA biosynthesis inhibitor paclobutrazol inhibits germination (Bentsink et al., 2006; Nakabayashi et al., 2012). Both ABA and DOG1 are essential for the establishment of seed dormancy, as the absence of either one is sufficient to abolish dormancy. However, they seem to function in parallel or partially independent pathways, because increased levels of either one cannot compensate for the absence of the other, as evidenced by the dog1 cyp707a2 mutant over-accumulating ABA and aba1–1 DOG1-Cvi combination harboring a strong DOG1 allele (Bentsink et al., 2006; Nakabayashi et al., 2012). Double mutant analysis demonstrated that dog1–1 enhanced the phenotype of the ABA insensitive mutant abi3–1 during Arabidopsis seed development, implying genetic interaction between AtDOG1 and ABI3 (Dekkers et al., 2016). In line with this, AtDOG1 has also been shown to interact with ABA HYPERSENSITIVE GERMINATION1 (AtAHG1) and AtAHG3, core ABA signaling components at both protein and genetic levels during seed dormancy induction and after-ripening mediated dormancy release (Nee et al., 2017; Nishimura et al., 2018). While AtAHG3 was inhibited by PYR/PYL/RCAR receptors in the presence of ABA, AtAHG1 was resistant to such inhibition in the same experimental context (Antoni et al., 2012). This suggests the ability of AtAHG1 to regulate ABA signaling distinct from the canonical PYR/PYL/RCAR - ABA pathway, which explains the need of AtDOG1 to suppress PP2C activity completely, and hence corroborates the indispensable roles of both ABA and DOG1 for dormancy establishment (Nee et al., 2017; Nishimura et al., 2018). Recently, ABI5-binding proteins (AFPs) were identified as downstream targets of the DOG1-PP2Cs module, thus forming an AtDOG1-AtAHG1-AtAFPs route to regulate Arabidopsis seed dormancy (Figure 3) (Krüger et al., 2025; Nee et al., 2017; Nishimura et al., 2018), which orchestrates the fact that AtAFP2, one of the main DOG1-PP2Cs targets, has been implicated in breaking primary seed dormancy by progressively silencing AtDOG1 (Deng et al., 2023). Although the seed dormancy phenotype of abi5 mutants resembles that of the wild type (Finkelstein, 1994), ABI5 plays key roles in ABA-mediated inhibition of germination of non-dormant seeds and post-germination growth arrest (Lopez-Molina et al., 2001, 2002). Recently, it has been shown that ABI5 acts downstream of DOG1 in this specific process (Nishimura et al., 2025).

Through sequence similarity and functional genetic approaches, significant progress has been made in characterizing DOG1 LIKE (DOGL) genes in cereals. However, our understanding of their roles in seed dormancy is far from complete (Table 2). First of all, most reported functional analyses were conducted using ectopic expression of cereal DOG1Ls in Arabidopsis or RNA interference mediated knockdown in cereals (Ashikawa et al., 2010, 2013; Ashikawa et al., 2014). It is anticipated that direct evidence would emerge from transgenic cereal lines or evolutionarily close model species such as Brachypodium (Scholthof et al., 2018). Moreover, AtDOG1 encodes a protein with no similarity to known proteins. How DOG1 and its homologous protein function remain unknown, though different hypotheses have been proposed. Most notably, the properties of AtDOG1 to undergo self-dimerization, bind heme, and interact with PP2Cs offer some clues to this puzzle, but more in-depth research would be required. Phylogenetic analyses indicate that DOG1 family genes contain different clades or groups in both Arabidopsis and cereals, but only limited members have been characterized (Ashikawa et al., 2013; Nishiyama et al., 2021). The function and possible involvement of those untouched ones in dormancy remain unknown (Figure 3). Interestingly, recent evidence in wheat seems to support the conserved role of DOG1Ls in seed dormancy through the AHG-PP2C module (Yu et al., 2020; Zhang et al., 2025c, 2025). Research in Arabidopsis showed that this module is required at various stages, including seed dormancy induction and dormancy release by dry after-ripening, but information of this kind in cereals remains unexplored (Nee et al., 2017).

Although seed dormancy has been extensively characterized at the genetic level, recent observations also reveal epigenetic regulation of this complex trait (Iwasaki et al., 2022; Tremblay and Qüesta, 2025). Through DNA methylation, chromatin remodeling and non-coding RNAs, epigenetic modifications regulate genomic imprinting, transcriptional gene silencing, developmental and environmental responses, thus contributing to coordinated seed development and fine-tuned seed dormancy (Figure 4).

The switch to germinate or stay dormant is fundamentally determined by the ABA/GA ratio and the sensitivity to these hormones, which is under strong environmental influence. Environmental signals, including water, light, temperature, nutrients and oxygen, serve as major inputs for seed germination. These signals reflect seasonal variation, time of the year, depth in the soil, shade, time of the day, soil composition, allelopathic compounds and competition around. A great deal of knowledge is present for Arabidopsis, which shows ecological similarities to most temperate cereals. However, evaluating genetic conservation in temperate cereals and finding genetic switches to fine tune dormancy requires further investigation. The relevance of different environmental factors, their ecological significance, and genetics are discussed in this section.

Gene and pathway discovery has always been at the forefront for understanding any trait, let alone seed dormancy. Various forward and reverse genetic approaches have been employed to achieve this purpose. In the past, forward genetic approaches like quantitative trait loci (QTL) analysis, genome wide association studies (GWAS) and mutant screens coupled with next generation sequencing have been frequently applied. With the ease of genome editing techniques like CRISPR, validation of homologs from Arabidopsis in temperate cereals and genetic improvement of PHS resistance have been accelerated. Here are a few examples.

The conserved central mechanism of ABA and GA hormonal balance triggered active attempts to modulate grain dormancy through manipulation of endogenous hormone content or signaling in wheat, barley, sorghum and rice (Ban et al., 2022; Fu et al., 2022; Gubler et al., 2008; Rodríguez et al., 2025). As metabolism and signaling genes showed a strong impact on the phenotypes, including deficiency in plant growth, drought resistance and seed development, it will be difficult to use these genes as direct breeding targets for PHS resistance. Moreover, these phytohormones play huge roles in overall growth, development and life history of the plant, so modification in these genes just for PHS resistance can come with a cost. Although it is still very relevant to study these genes for identifying some ideal targets present in the pathways.

After unrevealing dormancy specific genetic pathways of these genes, and utilizing other approaches, we were able to identify certain targets specifically related to seed dormancy in temperate cereals (Table 3). Some of these genes can be used as a potential target for improved PHS resistance.

In barley, targeted mutagenesis in Qsd1 (encodes an alanine aminotransferase, AlaAT) and Qsd2 (also called MKK3) revealed their essential roles in grain dormancy. In an Eastern Canadian barley biparental population LegCi, the non-dormant allele of Qsd1 was associated with reduced hypoxia stress sensitivity, which promotes grain germination (Farquharson et al., 2025; Sato et al., 2016). As hypoxia has been known to increase barley embryo sensitivity to ABA and interfere with ABA metabolism (Benech-Arnold et al., 2006), it would be of practical importance to determine whether this mechanism extends into other barley accessions and temperate cereals. Both qsd1, qsd2 single mutants and qsd1/qsd2 double mutant showed delayed germination, and qsd1 mutation partially suppressed the deep dormancy phenotype of qsd2 mutants (Hisano et al., 2022). Similarly, CRISPR/Cas9-induced triple-recessive mutation in the wheat homologue of Qsd1 resulted in a significantly deeper seed dormancy. In a field trial, the TaQsd1 mutants showed variable seed dormancy phenotypes, depending on genetic background and environmental conditions. Mostly, with the high maternal temperature and PHS susceptible background, a moderate dormancy phenotype was observed. This makes Qsd1 a controllable target for partial or complete loss of function to achieve an ideal PHS resistance phenotype.

Although no functional confirmation of TaMKK3 has been reported in wheat, the association of PHS with natural or mutagen-induced alleles indicated its potential usefulness for PHS resistance (Jørgensen et al., 2025; Martinez et al., 2020; Nakamura, 2018; Zhang et al., 2025a). Research on rice and barley MKK3 gene supports its conserved role as a negative dormancy regulator in cereals (Mao et al., 2019, 2024). As has been revealed to be involved in after-ripening, which is a controllable environmental switch (see section 7), the cereal MKK3 genes could be one of the most interesting targets for conferring controllable PHS resistance. However, knowledge gaps exist concerning the exact mechanism and strong phenotype of the knockout mutants, limiting the usefulness of knockouts for direct application.

Apart from MKK3, TaPHS1/TaMFT has been revealed to be a critical positive regulator of wheat PHS resistance by independent studies (Liu et al., 2013b; Nakamura et al., 2011). While gene expression analysis linked this gene with low temperature induced grain dormancy, its RNAi-mediated knockdown mutant showed PHS phenotype (Liu et al., 2013b). The PHS resistant allele has been introduced into durum wheat and triticale for significantly suppressed grain germination (Kato et al., 2017; Moullet et al., 2022). Studies on the two rice MFT genes, OsMFT1 and OsMFT2, reveal that the former promotes germination in the background of Nipponbare and Zhonghua 11, while the latter functions as a dormancy-promoter at least in the Zhonghua 11 cultivar, like TaMFT (Shen et al., 2024; Song et al., 2020; Zhang et al., 2025b). Intriguingly, another study in the Zhonghua 11 background found that OsMFT1 promotes seed dormancy, but no effect of OsMFT2 was observed (Lu et al., 2023). Thus, further investigation would be required to clarify the detailed role of OsMFT genes in regulating seed dormancy and germination in agronomically relevant genetic backgrounds under field conditions, which may pave the way for future application through overexpression or favorable allele stacking.

Another important target with potential for PHS resistance improvement could be DOG1. Its function and interactions with the environment and the hormonal pathway have been discussed in section 5. While potential interacting partners of DOG1Ls remain to be discovered in cereals, exploring other genes in this pathway could help to fine-tune seed dormancy levels. Moreover, despite the limited natural variation of DOG1 reported in temperate cereals (Nagel et al., 2019), it would be tempting to screen for natural variation of DOG1 using wheat landrace collection and identify functional alleles suitable for controlled dormancy (Pipatpongpinyo et al., 2020), which may serve as an interesting approach to address PHS under high seed development temperature. Another alternative could be DOG1 downstream factors, notably those involved in the DOG1-PP2Cs module. One compelling example could be the causal gene for a rice dormancy QTL SDR3.1, which encodes a mediator of OsbZIP46 deactivation and degradation (MODD) homologous to AtAFP acting downstream of the AtDOG1-AtAHG module (Guo et al., 2024).

Built on in-depth insights into the intricacy of seed dormancy and germination, pyramiding favorable alleles, genes, or QTLs would be feasible and worthwhile to achieve proper seed dormancy levels (Dong et al., 2025; Luo et al., 2021; Pipatpongpinyo et al., 2020; Wang et al., 2020a). At the same time, possible interactions between known dormancy regulators can be uncovered to find a more controllable dormancy switch. Additionally, the use of gene editing techniques to enhance or reduce the genetic expression of certain targets can be a helpful approach. As for pleiotropic trade-offs, targeting the most relevant domains and finding downstream targets in the context of PHS resistance is the way to go. Finally, to attain an ideal PHS phenotype, a model plant such as Brachypodium holds promise to fill the existing knowledge gaps.

Controlled seed dormancy in cultivated cereal varieties would be a sustainable solution to address pre-harvest sprouting. Conventional breeding and genetic modification could bring long-term solutions, especially in the context of a changing climate, which has been predicted to complicate the prospect of sprouting probability in dormancy-prone species.

Arabidopsis and temperate cereals contain several environmentally conserved mechanisms modulating seed dormancy, most notably the maternal effect, after-ripening and cold stratification, while only ABA/GA hormonal balance has been presented with consistent evidence supporting genetic conservation. However, obvious pleiotropic effects, namely its involvement in plant growth and development, make ABA/GA pathway a hard target to manipulate dormancy independently.

With respect to most of the environmental sensors and major dormancy regulators like DOG1, we still need to fill the remaining gaps concerning the genetic conservation between the two plant groups. In this context, Arabidopsis can serve as a template for initial hypothesis formation, but a robust and evolutionarily closer model system like Brachypodium could accelerate the efforts. Meanwhile, as a new frontier in crop breeding, we anticipate extensive investigation into the epigenetic regulation of seed dormancy and potential mitigation strategies for PHS. Another interesting avenue could be controllable resistance due to delayed germination rather than deep dormancy, which again warrants further in-depth study about the underlying intricacies of the environmental regulation aspects. We hope this manuscript can assist scientists in exploring untapped areas for effective PHS resistance.