The story of dopamine in plants is older than many researchers realise. The molecule was first detected in plant tissue in the saguaro cactus, where scientists observed a spike in endogenous dopamine within five minutes of tissue wounding, hinting at a protective role. Earlier work in 1958 had already identified catecholamines and serotonin in bananas, and dopamine was subsequently confirmed in banana peel and pulp, plantains and avocados. Bananas remain one of the richest known plant sources of the compound, and its antioxidant power there is striking: dopamine outperforms glutathione, ascorbic acid, catechin gallate and common synthetic antioxidants in free-radical scavenging assays. What has changed in recent years is the depth of mechanistic understanding, with studies now tracing dopamine’s effects from gene expression to whole-plant physiology.

Chemically, dopamine is identical across kingdoms. It is a benzene ring bearing two adjacent hydroxyl groups, the catechol moiety characteristic of catecholamines, attached to an ethylamine side chain. That catechol group is the secret of its antioxidant behaviour, donating electrons and hydrogen atoms to neutralise reactive oxygen species and, in some cases, chelating metals to disarm free radicals. The primary amine makes dopamine an organic base capable of forming salts in acidic conditions, while both functional groups hydrogen-bond readily with water, making the molecule highly polar. In animals, dopamine is synthesised from the amino acid tyrosine through a single route in which tyrosine hydroxylase acts as the rate-limiting enzyme. Plants, remarkably, run two alternative pathways: one decarboxylates tyrosine to tyramine via tyrosine decarboxylase before hydroxylation by monophenol hydroxylase, while the other hydroxylates tyrosine to L-DOPA first and then decarboxylates it with DOPA decarboxylase. Which route dominates depends on enzyme availability and plant species.

Inside the plant cell, dopamine appears to accumulate mainly in the vacuole, which serves as a storage compartment, with smaller quantities detected in the cytoplasm. Its production sites shift with need, from roots to leaves, and its concentration ranges from nanograms to micrograms depending on species and developmental stage. In opium poppy, dopamine is synthesised in young rosette leaves and declines as flowering begins. This spatial and temporal flexibility underscores a key theme of the review: dopamine is not a static metabolite but a dynamic, stress-responsive signal whose behaviour is tailored to the tissue, the species and the threat at hand.

The physiological reach of dopamine in plants is broad. Under stress, photosynthesis typically collapses as reactive oxygen species oxidise the pigments that capture light, forcing plants to close their stomata and conserve energy at the cost of growth. Dopamine intervenes at multiple points in this cascade. It stabilises the light-dependent reactions of photosynthesis, maintains stomatal conductance, preserves chlorophyll and supports optimal transpiration and carbon assimilation. In apple seedlings exposed to drought, a treatment of 100 micromolar dopamine enhanced net photosynthetic rate, relative water content, stomatal conductance and the content of chlorophyll a and b. Dopamine also reshapes root architecture, stimulating root vigour and elongation so that plants can explore soil for water and nutrients more effectively. Intriguingly, roots themselves secrete dopamine as a major exo-metabolite, suggesting it plays an active role at the root-soil-microbe interface.

At the molecular level, dopamine’s influence extends deep into gene regulation. Transcriptomic analysis of drought-stressed apple plants treated with dopamine revealed upregulation of calmodulin and calmodulin-like genes and cyclic nucleotide-gated channels involved in calcium signalling. The transient elevation of cytosolic calcium during stress initiates a cascade of adaptive cellular responses that activate downstream transcription factors, including MYBs and WRKYs. Because superoxide dismutase is a calmodulin-dependent enzyme, and glutathione peroxidase activation is also linked to calmodulin, dopamine’s calcium signalling effectively amplifies the plant’s antioxidant arsenal. The review also documents dopamine’s extensive crosstalk with phytohormones, including auxin, gibberellic acid, melatonin, abscisic acid, jasmonic acid and ethylene, fine-tuning the growth-defence trade-offs that determine how a plant allocates its limited resources under threat.

Each stress type reveals a different facet of dopamine’s versatility. Under salinity, exogenous dopamine in Malus hupehensis inhibited excess sodium and chloride uptake while enhancing the acquisition of potassium, nitrogen, phosphorus, sulphur, copper and manganese. Upregulation of genes such as MdHKT1, MdNHX1 and MdSOS1 shows dopamine engaging the salt overly sensitive pathway, the core salt-defence system in plants, pumping sodium into vacuoles and expelling it from root cells. In tomato seedlings, 100 micromolar dopamine maintained calcium-to-sodium and potassium-to-sodium ratios and produced striking gains: root dry weight increased by 286.84 percent, plant height by 108.37 percent and leaf area by 158.28 percent compared with untreated controls. Under cadmium stress in apple, dopamine reshaped the rhizosphere microbial community, enriching beneficial bacteria such as Frankia, Bradyrhizobium and Streptomyces and shifting keystone species in ways that helped the plant resist the metal.

Nitrogen stress and temperature extremes add further chapters. In cucumber grown under excess nitrate, 150 micromolar dopamine improved root growth, photosynthesis and antioxidant activity while upregulating genes for sucrose phosphate synthase, nitrate reductase and other enzymes that coordinate carbon and nitrogen metabolism. In apple, dopamine under low-nitrogen conditions increased expression of nitrate transporter genes and activated MdORG2, a transcription factor that boosts the plant’s own dopamine-synthesising machinery. Against cold, dopamine protected watermelon and grape seedlings by accumulating polyamines and osmolytes and bolstering antioxidant systems. Perhaps most commercially intriguing are the postharvest results: dopamine treatment significantly mitigated chilling injury in bananas stored at 7 degrees Celsius for 21 days and kiwifruits stored at 1 degree Celsius for 120 days, by activating the phenylpropanoid pathway, raising endogenous proline, GABA and glycine betaine, and preserving membrane integrity.

Dopamine also strengthens plant immunity against pathogens. In apple replant disease caused by Fusarium solani, 150 micromolar dopamine enhanced endogenous dopamine biosynthesis, reduced root damage and upregulated defence genes encoding chitinase and beta-1,3-glucanase, while increasing tyramine content and cell wall-bound amine deposition. Against Valsa mali infection in apple, resistance came through elevated phenolic content and salicylic acid. In pear, a foliar spray of 100 micromolar dopamine imparted resistance to Botryosphaeria dothidea by enhancing autophagy activity in host cells. Even allelopathic threats fall within its scope: dopamine counteracted phloridzin, a growth-inhibiting compound that disrupts apple rhizosphere communities, by lowering reactive oxygen species and enriching beneficial nitrogen-cycling microbes.

Significant gaps remain before dopamine can be deployed at scale. Research has concentrated on a narrow set of crops, chiefly apple rootstocks, tomato, cucumber and duckweed, while cereals, legumes and tropical fruits remain largely unexplored. Unlike in animals, no dopamine receptors have been identified or characterised in plants, leaving open the fundamental question of how the molecule is perceived. The threshold between beneficial and phytotoxic doses is poorly defined, and there is no regulatory framework governing exogenous dopamine use in agriculture. The review’s authors point to biotechnology as one promising route: overexpressing the tyrosine decarboxylase gene could raise endogenous dopamine levels and confer climate resilience without repeated spraying. Combined applications with melatonin, brassinosteroids and beneficial microbes offer further synergistic potential. If those mechanistic and safety questions can be answered, dopamine may graduate from laboratory curiosity to a next-generation regulator of crop resilience, extending its celebrated career from the animal brain to the world’s fields and orchards.

Subject of Research: The role of dopamine as a stress-regulating signalling molecule in plants

Article Title: Beyond neurotransmission: dopamine as an emerging biotic and abiotic stress regulator in plants

Article References: Shinde, D., & Pareek, S. (2026). Beyond neurotransmission: dopamine as an emerging biotic and abiotic stress regulator in plants. Stress Biology, 6(1), Article 24. https://doi.org/10.1007/s44154-026-00291-8

Image Credits: AI Generated

DOI: 10.1007/s44154-026-00291-8

Keywords: dopamine, plant stress, abiotic stress, biotic stress, antioxidant, reactive oxygen species, calcium signalling, phytohormones, salinity tolerance, drought tolerance, postharvest, plant signalling

The significance of this finding lies in the way it connects two domains of plant biology that have often been studied in isolation: hormone signalling and central carbon metabolism. Brassinosteroids are perceived at the cell surface by receptor complexes that ultimately inactivate a protein kinase called BIN2, a glycogen synthase kinase 3-like enzyme that functions as a central negative regulator of the brassinosteroid pathway. When brassinosteroid levels are low, BIN2 is active and phosphorylates a suite of targets, including transcription factors of the BZR1 family, thereby suppressing growth-related gene expression. When hormone levels rise, BIN2 is inhibited, its targets escape phosphorylation, and growth programmes are unleashed. The new work shows that this logic extends far beyond transcriptional control, reaching directly into the enzymatic core of sugar production.

PCK occupies a fascinating position in plant metabolism. In many plants, particularly those using C4 photosynthesis such as maize and sorghum, phosphoenolpyruvate carboxykinase catalyses the decarboxylation of oxaloacetate to release carbon dioxide and regenerate phosphoenolpyruvate, a step that concentrates carbon around the photosynthetic enzyme Rubisco and dramatically improves efficiency in hot, sunny climates. In other contexts, PCK drives gluconeogenesis, the synthesis of sugars from organic acids and lipid-derived carbon, which is essential during germination when seedlings must convert stored fat into the sugars needed to fuel early growth. In Arabidopsis, a C3 plant, PCK1 contributes to gluconeogenesis and to photosynthetic carbon metabolism, making the enzyme a versatile node at the intersection of energy production and carbon allocation.

The trail leading to the new discovery began with earlier proteomic work. A study by Tang and colleagues published in 2008 used prefractionation and two-dimensional difference gel electrophoresis to catalogue proteins whose modification changed after brassinosteroid treatment, and it revealed that PCK1 underwent dephosphorylation in response to the hormone. At the time, the observation was intriguing but mechanistically unexplained: it was not known which kinase placed the phosphate on PCK1, whether that modification affected enzyme activity, or whether the change mattered physiologically. The new study closes those gaps by identifying BIN2 as the kinase responsible and by showing that the phosphorylation event is functionally inhibitory.

A decisive piece of evidence came from a 2023 mapping effort by Kim and colleagues, who used TurboID-mediated proximity labelling coupled with mass spectrometry and phosphoproteomics to chart the signalling network of BIN2. That approach, which genetically fuses a promiscuous biotin ligase to BIN2 so that nearby proteins are labelled and can be identified, flagged PCK1 as a candidate substrate of the kinase. The new Nature Plants study builds directly on that lead, confirming that BIN2 physically interacts with PCK1, phosphorylates it at specific residues, and that this phosphorylation dampens the enzyme’s catalytic output. When brassinosteroids accumulate and BIN2 is restrained, PCK1 retains its unphosphorylated, active state, and sugar synthesis accelerates.

The physiological consequences of this regulatory module were tested across a remarkable evolutionary span. In Arabidopsis, the researchers manipulated brassinosteroid signalling and PCK1 phosphorylation status and observed corresponding changes in sugar accumulation. Strikingly, the same regulatory relationship held in maize and sorghum, two C4 grasses of enormous agricultural importance. The conservation of the BIN2–PCK1 module across such divergent species suggests that the coupling of brassinosteroid signalling to carbon metabolism is an ancient and fundamental feature of plant physiology rather than a quirk of a single lineage. For crop scientists, that conservation is encouraging news, because it implies that a single regulatory principle might be exploited to improve yield across cereals broadly.

The discovery also reframes a long-standing puzzle about how plants balance growth with carbon availability. Building new tissue requires both hormonal growth signals and an adequate supply of sugars, so plants need mechanisms that keep these two inputs in register. Recent work has shown that this coordination runs in both directions. In 2021, Zhang and colleagues reported that high sugar levels under light conditions can actually inhibit brassinosteroid signalling by enhancing BIN2-mediated phosphorylation of BZR1, providing a brake that prevents runaway growth when carbon status is already high. Conversely, the target of rapamycin pathway, a conserved nutrient-sensing network, promotes the accumulation of BZR1 in response to sugar, as shown in a 2016 study, thereby ensuring that sugar availability feeds positively into brassinosteroid signalling output.

Starvation adds a further layer of control. A 2025 study by Zhang and colleagues demonstrated that the ubiquitin ligase UPL3 mediates the degradation of BZR1 when nutrients run low, driving growth arrest and improving seedling survival under starvation stress. Taken together with the new findings, a coherent picture emerges: brassinosteroid signalling sits at the hub of a bidirectional dialogue with carbon metabolism, promoting sugar synthesis through PCK1 when conditions favour growth, while being restrained by sugar feedback and dismantled when carbon becomes scarce. The BIN2 kinase emerges as a shared bottleneck in this dialogue, phosphorylating both transcriptional regulators and metabolic enzymes to enforce the plant’s overall growth-versus-survival decision.

From a biotechnological standpoint, the implications are considerable. Enhancing PCK activity or reducing its inhibitory phosphorylation could, in principle, increase the efficiency with which crops convert carbon dioxide into sugars, the raw material for grain, biomass, and ultimately yield. Because the module operates in maize and sorghum, engineering or breeding strategies that favour the dephosphorylated, active state of PCK could be pursued in crops where even modest gains in photosynthetic efficiency translate into substantial harvest improvements. The finding also offers a mechanistic explanation for why brassinosteroid-related traits, such as enhanced seedling vigour, often correlate with improved performance in the field: the hormone is not merely stretching cells but also feeding the metabolic engine that powers growth.

As with any major advance, questions remain. The precise kinetic consequences of PCK1 phosphorylation at each target residue, the relative contributions of gluconeogenesis versus photosynthetic carbon concentration to the observed sugar increases, and the tissue-specific architecture of the BIN2–PCK1 module in developing seeds and leaves are all ripe for further study. It will also be important to determine whether tuning the module carries trade-offs, since unchecked sugar production could alter source–sink relationships within the plant. Nevertheless, by identifying a direct biochemical link between a growth hormone and a sugar-synthesising enzyme, the study transforms our understanding of how plants coordinate the decision to grow with the metabolic capacity to sustain it, and it hands crop engineers a concrete molecular target in the quest for more productive plants.

Subject of Research: Brassinosteroid hormone regulation of sugar synthesis through BIN2-mediated phosphorylation of phosphoenolpyruvate carboxykinase in plants

Article Title: Brassinosteroids boost sugar production by inhibiting PCK phosphorylation

Article References: Brassinosteroids boost sugar production by inhibiting PCK phosphorylation. (2026). Nature Plants, 12(9), 1673-1674. https://doi.org/10.1038/s41477-026-02378-6

Image Credits: AI Generated

DOI: 10.1038/s41477-026-02378-6

Keywords: brassinosteroids, BIN2 kinase, PCK, phosphorylation, sugar synthesis, gluconeogenesis, C4 photosynthesis, Arabidopsis thaliana, maize, sorghum, plant signalling, carbon metabolism

The story begins with a family of small peptides called C-TERMINALLY ENCODED PEPTIDES, or CEPs. When a root senses that the soil around it is deficient in nitrogen, it ramps up production of these peptide hormones, which travel through the xylem from the root to the shoot. High in the leaf phloem, these mobile peptides are detected by a receptor called CEP RECEPTOR 1, or CEPR1. This detection event is the pivot of the entire signalling cascade: it triggers the production of shoot-to-root mobile signals, including transcription factors known as CEPDs, that descend back into the roots and activate high-affinity nitrate transporters such as NRT2.1 in the roots that still dwell in nitrogen-rich patches of soil. The result is a beautifully compensatory system in which nitrogen-starved roots effectively recruit their better-positioned siblings to forage harder on behalf of the whole plant.

But there was a puzzle at the heart of this pathway. In other peptide hormone systems in plants, a single receptor kinase rarely acts alone. The classic example is the brassinosteroid pathway, where the receptor BRI1 requires its co-receptor BAK1 to achieve full signalling output. Co-receptors confer specificity, amplify signals, and often determine which downstream responses are engaged. Researchers therefore suspected that CEPR1, too, might depend on an as-yet-unidentified partner to translate CEP binding into the specific output of nitrogen-demand signalling. Yet years of genetic screening and biochemical analysis had failed to turn up such a partner, leaving the mechanism of CEP-dependent CEPR1 activation unknown.

The Nagoya University team, led by Yoshikatsu Matsubayashi with Mari Ogawa-Ohnishi and Taizo Nomura as co-first authors, took a biochemical approach to the problem. Using co-immunoprecipitation experiments in Arabidopsis thaliana, they searched for proteins that physically associate with CEPR1, but only in the presence of CEP peptides. This ligand-dependent interaction screen revealed a leucine-rich repeat receptor kinase that binds CEPR1 in a strikingly CEP-dependent manner. The protein, encoded by the gene At5g63710, belonged to a clade within leucine-rich repeat receptor kinase subgroup II that the researchers describe as the last functionally uncharacterized branch of that subgroup in Arabidopsis. They christened it CEP RECEPTOR INTERACTOR, CERI, reflecting both its discovery method and its molecular role.

Genetics quickly confirmed what biochemistry had suggested. Mutant plants in which the CERI gene was knocked out using CRISPR-Cas9 lost the ability to mount a systemic nitrogen-demand response. When the roots of these ceri mutants were starved of nitrogen, the leaves failed to properly induce the CEPD genes that normally relay the demand signal back down to the roots, and the compensatory boost in nitrate uptake in nitrogen-rich roots was impaired. Crucially, however, the loss of CERI did not disrupt every CEPR1-dependent function. The researchers showed that CEPR1-mediated regulation of root system architecture, a separate developmental response in which CEP signalling influences lateral root growth, remained intact in the ceri mutants. This dissociation was the key insight: CEPR1 can still signal without CERI, but only the systemic nitrogen-demand output requires the co-receptor.

That specificity is what makes CERI so interesting from a mechanistic standpoint. Rather than being a generic amplifier of all CEPR1 signalling, CERI appears to act as a specificity factor, selectively enabling one branch of the receptor’s output while leaving others untouched. This resembles the modular logic seen in other receptor kinase systems, where different co-receptors or phosphorylation patterns channel a single receptor into distinct cellular responses. The finding suggests that the architecture of plant peptide signalling is more layered than a simple ligand-receptor pair, and that the identity of the co-receptor can determine which physiological programme a receptor complex engages.

At the molecular level, the team dissected how CEP binding brings CEPR1 and CERI together and what happens next. Using mass spectrometry, they mapped phosphorylation sites on both proteins and found that CEP treatment triggers phosphorylation of the activation loops of both CEPR1 and CERI, the regulatory segments that must be phosphorylated for a kinase domain to become catalytically active. This pattern of CEP-dependent transphosphorylation is a hallmark of receptor kinase complex activation, mirroring the sequential phosphorylation events described for the BRI1-BAK1 brassinosteroid complex. Mutations that eliminate these activation-loop phosphorylation sites abolish signalling, confirming that the kinase activities of both proteins are essential. In other words, CEP binding assembles an active receptor kinase duo, and the coordinated phosphorylation of both partners is what generates the intracellular signal that ultimately commands the roots to take up more nitrate.

The evolutionary dimension of the work adds further resonance. CEP peptides and their signalling pathways are specific to seed plants, and the genomes of nonflowering land plants have revealed how peptide signalling expanded over the course of plant evolution. Identifying CERI as the functional co-receptor for nitrogen-demand signalling not only completes the circuit in Arabidopsis but also provides a reference point for tracing how this sophisticated long-distance communication system was assembled over hundreds of millions of years. Because the CEP-CEPR1 pathway also intersects with plant immunity, with recent work showing that CEP signalling coordinates immune responses with nitrogen status, understanding the receptor complex at atomic and genetic resolution has implications well beyond nutrient physiology.

The practical stakes are considerable. Nitrogen fertilizer underpins modern agriculture, but applied nitrogen is notoriously inefficient: a large fraction is lost to leaching, volatilization, and denitrification, polluting waterways and generating the potent greenhouse gas nitrous oxide. A crop plant with a sharpened nitrogen-demand signalling system could, in principle, fine-tune its uptake more precisely to what it actually needs, absorbing nitrates more efficiently when and where they are available. Because CERI specifically gates the systemic demand response without interfering with other developmental functions of CEPR1, it offers an appealing target for breeding or genome editing: enhancing CERI-dependent signalling could boost nitrogen use efficiency while leaving root architecture and other CEP-dependent traits unaltered. The Nagoya team’s work, rooted in fundamental curiosity about how plants talk to themselves, thus delivers both a completed signalling circuit and a candidate molecular lever for one of agriculture’s most pressing challenges. The raw mass spectrometry data underlying the study have been deposited in the ProteomeXchange consortium via the jPOST repository, and the Arabidopsis lines generated in the study are available from the corresponding author, ensuring that other laboratories can immediately build on this newly completed map of the plant nitrogen-demand circuit.

Subject of Research: Systemic nitrogen-demand signalling in plants via the CEP-CEPR1-CERI receptor kinase pathway

Article Title: An LRR co-receptor kinase essential for systemic nitrogen-demand signalling

Article References: Ogawa-Ohnishi, M., Nomura, T., Hayashi, Y., Yamashita, Y., Noda, S., Suda, R., Ohkubo, Y., & Matsubayashi, Y. (2026). An LRR co-receptor kinase essential for systemic nitrogen-demand signalling. Nature Plants. https://doi.org/10.1038/s41477-026-02391-9

Image Credits: AI Generated

DOI: 10.1038/s41477-026-02391-9

Keywords: CERI, CEPR1, CEP peptides, nitrogen-demand signalling, leucine-rich repeat receptor kinase, co-receptor, Arabidopsis thaliana, nitrate uptake, plant signalling, root architecture, nitrogen use efficiency, Nature Plants