At the heart of the system sits a hormonal tug-of-war between two antagonistic phytohormones. Abscisic acid (ABA) enforces and maintains dormancy, while gibberellins (GA) promote germination. Crucially, the review emphasizes that the ratio between the two hormones, rather than their absolute concentrations, determines seed fate. When ABA dominates, biosynthetic enzymes such as NCED6 and NCED9 ramp up production and downstream transcription factors like ABI3, ABI4 and ABI5 lock the seed into a protected, metabolically restrained state. When GA dominates, DELLA proteins—the master nuclear growth repressors, most prominently RGL2 in seeds—are marked for destruction by the ubiquitin-proteasome machinery after binding the GA receptor GID1. Removing RGL2 simultaneously dismantles ABA signaling, since the DELLA protein is needed to sustain ABI5 expression, and thereby liberates the transcriptional programs for cell elongation and the cell-wall-loosening enzymes that allow the radicle to physically break through the seed coat.

Light is the central environmental signal that tips this seesaw. Seeds sense the red-to-far-red ratio of the light reaching them, a measurement that reveals whether they lie buried in deep soil, where red light is filtered out, or near the surface under an open sky. The photoreceptor phytochrome B absorbs red light at roughly 660 nanometers and converts to its active Pfr form, which migrates into the nucleus and binds PHYTOCHROME-INTERACTING FACTOR 1 (PIF1), a transcription factor that functions as the pivotal molecular switch. In darkness, PIF1 accumulates and orchestrates a dormancy program: it activates ABA biosynthetic genes, suppresses the ABA catabolic gene CYP707A2, represses GA biosynthesis through GA3ox1 and GA3ox2, upregulates the GA-deactivating gene GA2ox2, and switches on the DELLA genes GAI and RGA. Red light triggers rapid proteasomal degradation of PIF1, reversing the entire hormonal landscape within hours—a shift toward GA dominance that commits the seed to germinate.

The review details how PIF1 is embedded in an expanding network of interacting regulators. In darkness, PIF1 partners with ABI5 in a synergistic complex that boosts each protein’s DNA-binding power, driving expression of germination inhibitors such as SOMNUS and DAG1 while silencing growth genes. A feedback loop between PIF1 and the MYB-like factors REVEILLE1 and REVEILLE2 amplifies dormancy signals, with RVE1 directly repressing GA3ox2 and physically stabilizing RGL2 by blocking its E3 ligase SLY1. Meanwhile, proteins PCH1 and PCHL prolong the active state of phytochrome B, suppressing its dark reversion so that even brief flashes of light can push a seed past the physiological threshold for commitment. Beyond ABA and GA, genome-wide binding studies show that PIF1 also rewires auxin, jasmonate, ethylene, brassinosteroid, cytokinin and strigolactone pathways, establishing a layered molecular barrier against premature germination under any unfavorable condition.

Other environmental inputs converge on the same ABA–GA axis. Temperature programs dormancy depth through DELAY OF GERMINATION 1 (DOG1), and remarkably, a mother plant’s thermal history can be transmitted to her offspring via the mobile FLOWERING LOCUS T protein, which travels from leaf veins into developing seed coats and softens dormancy by altering tannin biochemistry. Soil nitrate, sensed through the dual-affinity transporter NRT1.1 and tuned by the kinase CIPK23, promotes germination by downregulating DOG1 and upregulating GA3ox1. Even fire plays a role: karrikins in smoke, perceived through the KAI2 receptor, and endogenous strigolactones, perceived through D14, both recruit the F-box protein MAX2 to degrade SMAX1 and SMXL2 repressors, tilting the hormonal balance toward germination. Parasitic Striga weeds have exploited this circuit with duplicated, ultrasensitive KAI2 receptors that detect host-exuded strigolactones at picomolar concentrations. Soil compaction works in the opposite direction, creating hypoxia that blocks ABA breakdown and maintains a high ABA-to-GA ratio until mechanical resistance falls.

The most provocative part of the framework concerns the epigenome. Transient transcription factor binding alone cannot explain how a fleeting light exposure produces a stable developmental decision. The review compiles evidence that DNA methylation, histone modifications, chromatin remodeling and small RNAs convert environmental signals into lasting or reversible chromatin states. CHH methylation, for instance, accumulates during seed development and is then substantially lost during germination, accompanied by chromatin opening and the removal of repressive marks. A particularly elegant example links light directly to histone chemistry: upon red-light-induced PIF1 degradation, the repressor SOMNUS is silenced, releasing the JmjC-domain demethylases JMJ20 and JMJ22, which strip the repressive H3K9me2 mark from the GA3ox1 and GA3ox2 loci and physically unlock GA biosynthesis. Light, in effect, rewrites the histone code to write the germination program.

Additional epigenetic layers reinforce or release dormancy. The DNA demethylase ROS1 controls maternal imprinting of the germination-promoting gene DOGL4 in Arabidopsis, and comparative methylomes in wheat reveal differential methylation of GA20ox, NCED, PP2C and SnRK2 genes associated with pre-harvest sprouting resistance. Polycomb Repressive Complex 2 deposits H3K27me3 to lock away vegetative growth genes in dormant embryos, with rice homologs OsEMF2b and OsFIE1 demonstrating that this silencing system governs dormancy in cereals as well. The SWI2/SNF2 ATPase BRAHMA counters Polycomb repression by repositioning nucleosomes at target promoters. Small RNAs add yet another dimension: miR156, maintained high by DOG1 during dormancy, prevents phase transition, while rice engineered to elevate miR156 shows enhanced dormancy and reduced pre-harvest sprouting with minimal yield trade-offs. Wheat miR9678 suppresses germination by generating phased small interfering RNAs from a long non-coding RNA precursor.

The translational implications for agriculture are considerable. Domestication has weakened primary dormancy in cereals to guarantee rapid, uniform field emergence, but this has made modern wheat and barley vulnerable to pre-harvest sprouting, in which rain triggers premature germination on the ear and hydrolytic enzymes destroy starch and protein quality. Because the upstream phyB–PIF1 circuitry and the core ABA–GA modules are broadly conserved, the review argues that fine-tuning light-responsive germination thresholds—potentially through DOG1-like genes, histone modifiers or microRNA pathways—offers a route to sprouting-resistant cultivars without sacrificing establishment. Single-cell transcriptomics adds a final wrinkle: germination is asynchronous at the cellular level, and cell-to-cell differences in chromatin state may buffer populations against unfavorable conditions, a form of bet-hedging written in epigenetic variation.

Significant gaps remain. The precise molecular links connecting photoreceptor activation to chromatin modifiers such as BRAHMA and REF6 are still unknown, as is the extent to which maternal light quality shapes seed chromatin across generations. Most functional work on cereal DOG1-like genes has relied on indirect expression studies, and the spatial orchestration of light-induced epigenetic changes across embryo, endosperm and seed coat has yet to be mapped. The authors call for single-cell and spatial omics combined with live imaging and computational modeling to resolve these dynamics. What the review makes unmistakably clear, however, is that a seed’s decision to grow is not a simple response to water and warmth. It is the output of a coordinated multilayered network in which photons, hormones and chromatin converge—ensuring that life begins only when the world is ready to receive it.

Subject of Research: Light, hormone and epigenetic regulation of seed dormancy and germination

Article Title: Seed germination: light-hormone-epigenome crosstalk at the dormancy-to-growth transition

Article References: Kushwah, S., Sharma, S., & Kumar, V. (2026). Seed germination: light-hormone-epigenome crosstalk at the dormancy-to-growth transition. Frontiers in Plant Physiology, 4, Article 1870445. https://doi.org/10.3389/fphgy.2026.1870445

Image Credits: AI Generated

DOI: 10.3389/fphgy.2026.1870445

Keywords: seed dormancy, germination, phytochrome, PIF1, abscisic acid, gibberellins, epigenetics, chromatin remodeling, pre-harvest sprouting, crop resilience, Seed, light-hormone-epigenome

The study, published in Plant Cell Reports, began with a careful comparison of two quinoa lines that behave very differently in the field. The researchers observed that the variety R157 showed significantly greater resistance to pre-harvest sprouting than the line S222. This natural contrast provided a powerful experimental system: by dissecting what distinguishes a seed that stays dormant from one that germinates prematurely, the team could trace the physiological and molecular differences that underpin resistance. Their measurements revealed that resistance to pre-harvest sprouting in quinoa is closely tied to the balance of two key plant hormones, gibberellin and abscisic acid, as well as to amylase activity and the rate of starch metabolism within the seed.

The hormonal tug-of-war at the heart of seed behavior is well documented in plant biology. Gibberellin promotes germination by stimulating the production of enzymes that break down stored starch into sugars that fuel the emerging seedling. Abscisic acid, by contrast, enforces dormancy and counteracts germination. When rain soaks a mature crop, the balance between these hormones can tip, amylase enzymes surge, starch reserves are dismantled and the seed commits to germination whether or not the farmer is ready. Understanding which genes control this switch in quinoa has been a persistent challenge, because the crop’s large, complex genome has only recently become accessible to detailed genetic analysis.

To find the regulators responsible, the team turned to weighted gene co-expression network analysis, a computational method that scans thousands of genes measured across different conditions and clusters those that rise and fall together. Genes that move in concert often participate in the same biological process, and the technique frequently pinpoints master regulators hidden within large transcriptomic datasets. In this case, the analysis converged on a striking candidate: a transcription factor called CqRVE5, a member of the REVEILLE family of genes, together with its predicted target gene, CqHAI3. Both genes emerged as central hubs associated with pre-harvest sprouting resistance in quinoa.

Follow-up characterization showed that CqRVE5 and CqHAI3 share remarkably similar expression patterns, with both preferentially active in seeds rather than in leaves, stems or roots. When the researchers tagged the corresponding proteins with fluorescent markers, both were found to localize to the nucleus, the expected destination for proteins that regulate gene expression. These features are consistent with a role in which CqRVE5, acting as a DNA-binding transcription factor, directly controls the activity of CqHAI3 within seed tissue, where the decision to germinate or remain dormant is ultimately made.

To test whether these genes actually influence germination, the team overexpressed each of them in Arabidopsis thaliana, the standard laboratory workhorse of plant genetics. The results were unambiguous. In transgenic seeds carrying either CqRVE5 or CqHAI3, the levels of gibberellin relative to abscisic acid shifted, amylase activity declined and the rate of starch degradation slowed. The consequence was a measurable reduction in germination capacity. In other words, both genes act as negative regulators of seed germination, holding the seed back from sprouting. This finding directly links the gene pair to the physiological traits, hormone balance, starch breakdown and germination vigor, that determine whether a quinoa seed sprouts on the plant.

The researchers then probed the relationship between the two genes at the molecular level. Using promoter-binding assays, they demonstrated that the CqRVE5 protein can bind to specific sequences in the promoter region of the CqHAI3 gene and activate its expression. This establishes CqHAI3 as a direct downstream target of CqRVE5, forming a coherent regulatory module rather than two genes acting in parallel. The architecture is notable because CqHAI3 belongs to a family of protein phosphatases associated with abscisic acid signaling, suggesting a mechanism in which a circadian-linked transcription factor reinforces the dormancy-promoting arm of hormone signaling precisely when the seed reaches harvest maturity.

The implications for agriculture could be substantial. Pre-harvest sprouting is a major problem not only in quinoa but also in wheat, barley and rice, where it degrades grain quality and costs growers billions of dollars worldwide. In wheat, breeders have long sought genes that maintain dormancy through wet harvests, and several regulatory modules have been characterized in cereals. The identification of the CqRVE5-CqHAI3 module adds a new piece to this puzzle and proposes a previously unappreciated mechanism for sprouting control in a crop whose genome is unusually complex. Because the module suppresses germination by influencing starch metabolism through hormone pathways, it offers a clear entry point for marker-assisted selection or genome editing aimed at enhancing dormancy without compromising other agronomic traits.

There are, of course, important caveats. The functional evidence for the module comes primarily from overexpression studies in Arabidopsis, a distantly related species, and from correlation-based network analysis in quinoa itself. Confirming that the same module operates in quinoa seeds under field conditions will require additional experiments, such as knockout or knockdown of the genes in quinoa and testing across diverse germplasm and environments. The authors also note that resistance to pre-harvest sprouting is a quantitative trait shaped by multiple genes, seed coat structures and environmental factors, so the CqRVE5-CqHAI3 module is best viewed as one key component of a broader regulatory network rather than a single master switch.

Even with those qualifications, the study represents a meaningful advance for a crop whose global importance is rising rapidly. As demand for plant protein grows and climate variability makes harvest-season weather increasingly unpredictable, protecting quinoa from pre-harvest sprouting becomes both an economic and a food-security priority. By tracing the trait from a resistant variety through hormone physiology, starch biochemistry and a defined transcriptional cascade, the Gansu team has delivered a mechanistic framework that breeders and molecular biologists can now build upon. If subsequent work validates the module in elite quinoa lines, the humble grain’s tendency to wake up too soon could finally be switched off, at the level of its own DNA.

Subject of Research: The CqRVE5-CqHAI3 gene module regulating pre-harvest sprouting resistance in quinoa seeds.

Article Title: CqRVE5-CqHAI3 is the potential key gene module regulating pre-harvest sprouting in quinoa

Article References: Wang, X., Wang, B., Liu, W., Zhao, Y., Zhu, X., Wang, Y., Chai, J., Liu, H., & Wei, X. (2026). CqRVE5-CqHAI3 is the potential key gene module regulating pre-harvest sprouting in quinoa. Plant Cell Reports, 45(10), Article 287. https://doi.org/10.1007/s00299-026-03971-x

Image Credits: AI Generated

DOI: 10.1007/s00299-026-03971-x

Keywords: quinoa, pre-harvest sprouting, seed germination, CqRVE5, CqHAI3, abscisic acid, gibberellin, starch metabolism, transcription factor, seed dormancy, WGCNA, Plant Cell Reports