Plants exhibit diverse regeneration strategies to heal wounds, regrow organs, and clonally propagate. These regeneration strategies depend on inductive cues such as wounding, stress or hormones initiating cell division and cell differentiation. However, wounding activates both regeneration and defence responses, and it has become clear that plants actively decide when to regenerate and what to regenerate. By integrating cell wall, hormonal, mechanical and environmental cues, plants can initiate and shape diverse regeneration outcomes such as callus formation, root regeneration, grafting and shoot formation. Here, we discuss the latest developments in how plants activate regeneration and establish a multitude of diverse regeneration outcomes. We focus on the diversity of regeneration, the trade-off between defence and regeneration, the role of signalling in fate determination and how external cues promote regeneration plasticity. Such knowledge has implications for better understanding the adaptive relevance of regeneration and for modifying fate outcomes to enhance biotechnological applications of plant regeneration.
Shoot branching, a major determinant of plant architecture and productivity, has long been attributed to the coordinated action of auxin, cytokinins (CKs), and strigolactones (SLs). Recent work shows that sugars act not only as metabolic resources but also as early developmental signals that regulate axillary bud outgrowth, the initial step in shoot branching. Sugar availability can rapidly trigger bud outgrowth, often preceding major hormonal changes. Mechanistically, sugars antagonize auxin and SL signaling while acting synergistically with CKs. These effects involve sugar signaling pathways mediated by trehalose 6-phosphate (Tre6P) and HEXOKINASE1 (HXK1), as well as metabolic reprogramming of glycolysis, the tricarboxylic acid (TCA) cycle, and the oxidative pentose phosphate pathway (OPPP). The transcription factor BRANCHED1/TEOSINTE BRANCHED1 (BRC1/TB1) participates in this regulatory network by integrating specific sugar and hormonal inputs involved in the control of the transition between bud dormancy and bud outgrowth. Here, we synthesize current knowledge on the interplay between sugar metabolism, sugar signaling, and hormonal pathways in regulating bud fate and highlight key questions that will shape future research in this field.
Drought triggers reprogramming of sugar transport, which acts as a central hub linking stress perception to carbon allocation. Under drought, FERONIA acts as a cell wall-plasma membrane turgor sensor that activates SnRK2s via outside-in signaling, and stress-activated kinases (SnRK2s, CPKs, and CIPKs) directly phosphorylate SWEET, SUT1, and TST transporters to enhance long-distance sucrose transport and vacuolar sugar accumulation. Recent cross-species single-cell atlases have identified phloem foundational genes as new targets for improving sugar transport. Meanwhile, deep mutational scanning enables high-throughput screening for SWEETs with enhanced sucrose transport activity. Remaining challenges include the need for characterization of sugar unloading in sink tissues. Thus, sugar transport integrates drought perception with metabolic adjustment, providing principles for engineering carbon partitioning under drought.
As the outermost epidermal structures, trichomes mediate plant-environment interactions and play critical roles in plant adaptation and stress responses. Beyond providing physical protection, many trichomes develop specialized glandular structures capable of biosynthesizing a diverse array of secondary metabolites with defensive functions. In addition, these compounds derived from glandular trichomes (GTs) also possess substantial economic value. Elucidating the regulatory mechanisms governing GT development is therefore essential for improving plant stress tolerance and for harnessing synthetic biology to produce high-value compounds. In this review, we highlight recent advances in understanding GT morphogenesis and discuss major challenges and future directions in the field.
Identifying transcriptional regulators that control important biological pathways in plants is fundamental to understanding regulatory mechanisms, network hierarchy, and phenotypic variation. This remains challenging because transcription factors (TFs) and their targets operate within highly interconnected, dynamic, and often redundant regulatory networks. Over the past two decades, advances in omics technologies, sequencing data generation, and computational tools have shifted gene discovery from single-gene studies to network-level investigation. At the same time, these advances have created a new challenge: how to extract biologically meaningful regulatory relationships from increasingly complex and high-dimensional datasets. Recent progress in multi-omics integration and artificial intelligence (AI), including machine learning (ML), deep learning, and emerging foundation-model approaches, is beginning to address this challenge and is reshaping how transcriptional regulators, targets, and regulatory relationships are predicted in plants. In this review, we summarize advances in network-enabled gene discovery, discuss how multi-omics and AI are transforming transcriptional target prediction, and consider how these developments may lead to predictive models of plant gene regulation with applications in crop improvement and synthetic biology.
Spray-induced gene silencing (SIGS) has moved from proof-of-concept to one of the most compelling RNA-based routes for crop protection, yet its field deployment still rests on unresolved biological interfaces. In this review, we revisit SIGS against fungal pathogens by asking where exogenous double-stranded RNAs go, which organisms perceive them, and how delivery technologies may reshape their ecological footprint. We first examine double-stranded RNA (dsRNA) uptake as a limiting and still unevenly understood step: clathrin-mediated endocytosis is emerging as a recurrent entry route in fungi, whereas plant perception, transport across surface barriers, and systemic movement remain mechanistically obscure. We then discuss evidence that dsRNAs are not inert silencing triggers. Beyond sequence-specific RNA interference, they can activate pathogen-associated molecular pattern (PAMP)-like and stress-response pathways, including fungal high osmolarity glycerol (HOG) signaling, implying that dose, formulation, and exposure context may influence both efficacy and nontarget effects. This perspective is extended to the plant holobiont, where direct off-target silencing and indirect microbiome remodeling represent distinct but often conflated risk layers, particularly for endophytic and beneficial fungi exposed through systemic RNAi. Finally, we evaluate how nanocarriers, BioClay, chitosan particles, and artificial vesicles are being developed to protect dsRNAs from degradation, improve uptake and enable more precise delivery. We argue that the next phase of SIGS research must integrate molecular uptake biology, concentration-aware risk assessment, and scalable formulation design. Such integration will determine whether SIGS becomes merely another promising laboratory technology or a robust, ecologically informed platform for sustainable fungal disease management in agriculture.
Carbon (C) and nitrogen (N) availability must be continuously integrated to sustain plant growth and development, yet the molecular mechanisms underlying this integration have long remained elusive. In this review, we highlight emerging evidence that C and N signaling converge on a regulatory network involving SnRK1, NLP7, TOR, and potentially nitric oxide. The clearest conceptual advance is the demonstration that SnRK1 directly phosphorylates the nitrate sensor and transcriptional regulator NLP7, providing an integration node through which energy limitation and C deficiency can suppress the primary nitrate response. SnRK1 activity is modulated by C status and the sucrose-specific signaling metabolite trehalose 6-phosphate, and by nitrate availability through HOS1-dependent regulation of KIN10 abundance. In parallel, nitric oxide is emerging as a key signal at the interface of nitrate assimilation, mitochondrial activity, sucrose responses, and TOR activation. The discovery of additional regulatory layers suggests that C/N integration is organized as interconnected signaling modules rather than single linear pathways. We further discuss how these signaling interactions are involved in plant metabolism and development. By coordinating nitrate assimilation with tricarboxylic acid cycle activity, redox metabolism, and C skeleton availability, C/N signaling aligns C anabolic capacity with N supply. These effects extend to developmental outputs, including meristem activity, root growth, shoot branching, and flowering. Together, these findings support a shift from viewing C and N signaling as parallel pathways to considering them as a unified regulatory system for metabolic and developmental plasticity.
Plant-microbe interactions are spatially organized processes. Increasing evidence suggests that nutrients play a critical role in this organization by not only acting as resources but also as spatial signals. In plants, nutrient perception and signaling are spatially patterned across tissues, while in microbes, local nutrient conditions guide colonization, metabolism, and function. These responses create heterogeneous interaction niches at the plant-microbe interface, but how they are coordinated across individual cells remains unclear. Recent advances in single-cell, spatial omics and nutrient mapping approaches now enable these processes to be resolved at cellular resolution. Here, we bring together current understanding of nutrient-guided plant and microbial responses and highlight emerging technologies that allow their integration. We then introduce a cell-state framework to interpret plant-microbe interactions as emergent properties of spatially coupled cellular responses linked through local chemical environments. This perspective provides a foundation for a more mechanistic and predictive understanding of plant-microbe interactions.
Abscisic acid (ABA) coordinates plant development and water-stress responses through mechanisms that extend beyond local biosynthesis and signaling. Increasing evidence indicates that ABA function depends on the spatial organization of hormone production, transport, catabolism, and perception across tissues. In this review, we highlight how ABA is synthesized mainly in vascular-associated cells and redistributed to distal target sites in leaves, roots, and seeds. We discuss recent findings showing that both ABA and its precursor, abscisic aldehyde, can move between tissues, thereby expanding the routes by which bioactive hormones accumulate. We further consider how transporters, tissue-specific sinks, and environmental cues shape ABA gradients, and highlight outstanding questions regarding the cellular pathways and regulatory mechanisms that determine ABA action in planta.
Selective autophagy has emerged as a central interface in plant–virus interactions, acting at once as an antiviral defense, a proviral vulnerability, and a regulator of host immune homeostasis. In plants, autophagy can directly target viral proteins, replication complexes, and even entire virions for degradation, while viruses have evolved diverse strategies to exploit, evade, or repurpose the autophagy machinery. Recent work has revealed an expanding repertoire of plant- and virus-encoded selective autophagy receptors, as well as unexpected roles for autophagy in restraining excessive immune activation and tissue damage during infection. These findings challenge a binary classification of autophagy as either antiviral or proviral. Here, we synthesize recent advances in the field and propose a conceptual framework in which multiple selective autophagy pathways operate in parallel during viral infection, each targeting distinct viral or host components and collectively shaping infection outcomes.
Structural biology is undergoing a transformative era driven by advances in artificial intelligence (AI)-based protein structure prediction and cryo-electron microscopy. Predictive approaches have dramatically expanded structural coverage across proteomes and are increasingly integrated into experimental workflows. However, protein function frequently depends on dynamic molecular processes including ligand-dependent conformational remodeling, transient interactions, cooperative assembly, and transport-state transitions that remain difficult to define from static computational models alone. These challenges are particularly evident in plants, where signaling pathways often involve environmentally responsive receptor complexes, lineage-expanded regulatory proteins, and transient assemblies. Here, we discuss how experimental structural biology continues to advance plant biology by revealing mechanisms underlying hormone perception, immune receptor activation, transporter function, and enzymatic regulation. From early landmark discoveries such as the crystallization of urease to recent cryo-electron microscopy studies of dynamic signaling complexes, plant systems have repeatedly uncovered molecular architectures, chemically modified intermediates, and regulatory principles that require direct structural and biochemical characterization. Plant proteins also remain markedly underrepresented in structural databases, leaving many plant-specific pathways structurally unresolved. Together, these observations highlight the continuing importance of experimental structural biology for defining biologically relevant molecular states and enabling structure-guided strategies for crop improvement and agricultural biotechnology.
Arbuscular mycorrhiza (AM) represents a key strategy for plants to overcome nutrient starvation. In legumes and rice, the development of this symbiosis requires the GRAS transcription factor DELLA, previously identified as central proteolytic target of gibberellin (GA) signaling. DELLA performs critical functions across multiple stages in AM development, including inner root cortex patterning, arbuscule initiation and degeneration, by regulating essential downstream genes driving these phenomena. Moreover, DELLA appears as a regulatory hub that integrates hormonal signals, environmental stimuli, and symbiosis formation. Here, we highlight recent advances in our understanding of DELLA-mediated regulation of AM development and provide state-of-the-art insights into how DELLA orchestrates these signaling pathways.
Natural de novo shoot organogenesis (DNSO) is the spontaneous regeneration of shoots from wound sites outside the shoot apical region through endogenous developmental programs. This regenerative capacity enables plants to recover from severe tissue damage by re-establishing the shoot-root axis. Here, we review current knowledge about the molecular mechanisms of natural DNSO, focusing on transcriptomic and physiological studies in model plants. Accumulating evidence suggests that natural DNSO proceeds through three sequential phases: (i) early wound responses, characterized by the activation of the WIND1-ESR1 module and the establishment of apical-basal auxin asymmetry; (ii) cellular proliferation driven by metabolic and cell-cycle reprogramming; and (iii) cytokinin-mediated establishment of shoot apical meristem identity. We also discuss how these mechanistic insights have been harnessed for practical applications, including tissue culture-free transformation systems such as the cut-dip-budding (CDB) method, and developmental reprogramming strategies that employ ectopic expression of developmental regulator (DR) genes to induce DNSO in otherwise recalcitrant species. Together, these advances illustrate how understanding natural regeneration can guide the development of simplified, broadly applicable plant transformation technologies.
The root endodermis forms a selective interface between the soil environment and the vasculature, which is essential for radial transport. Traditionally defined by its barriers, it is increasingly understood that the endodermis is a dynamic tissue in which development, cell wall modification, and signaling are integrated. Moreover, evidence is emerging that this tissue contains several cell files with individual identity, which may play distinct physiological roles in integrating environmental responses. Based on this, we present here a spatiotemporal perspective on endodermal function, following its progression from early specification to eventual termination during secondary growth. We give an overview of the endodermal life cycle, from early specification and barrier differentiation to its eventual replacement during secondary growth. We propose that the endodermis functions as a transient regulatory interface in which cell identity programs, positional cues, barrier surveillance pathways, and environmental responses converge to control transport and signaling. In this view, the endodermis is not simply a passive diffusion barrier, but a developmentally patterned, tunable tissue that actively adjusts radial permeability during root growth. Its influence extends beyond its lifespan, shaping subsequent developmental trajectories and plant–environment interactions.
Vascular plants distribute reducing power among organelles, cells, and tissues in the form of malate, a stable metabolite from which organisms can quickly generate the strong reductants NADH and NADPH. Current thought is that malate in chloroplasts derives either from the import and reduction of oxaloacetate or from the import of malate into chloroplasts via an exchange with glutamate. This article proposes that plastid malate may also derive from rubisco-mediated catabolism of RuBP to pyruvate, followed by the putative conversion of pyruvate to malate through two alternative pathways. One pathway involves the enzymes phosphogluconate dehydrogenase and malic enzyme, and the other involves PEP carboxylase and malate dehydrogenase. These enzymes have metal-binding sites that accommodate either manganese or magnesium, but association with manganese favors malate generation. Therefore, plants may shift the balance between manganese and magnesium activities in chloroplasts to enhance malate generation for nitrate and sulfate assimilation into amino acids at the expense of carbon fixation and carbohydrate accumulation. This regulatory mechanism may help plants maintain protein homeostasis as atmospheric CO2 rises in the coming decades.
Plant architectural innovations have been fundamental in improving plant production. With a changing climate, salt stress is an increasing threat to agricultural production, but if and how plant architecture contributes to salt tolerance remains unclear. We review recent studies on the regulation of (lateral) root, root hair, flower development, halotropism and shade avoidance during salt stress and formulate a plant model that brings together architectural and physiological features contributing to salt tolerance. The review highlights open questions on the role of plant architecture in salt tolerance and offers a starting point for developing a salt-tolerant ideotype.
The lipid-derived phytohormone JA-Ile is a critical regulator of environmental and developmental responses in flowering plants. This signaling molecule protects plants against biotic and abiotic challenges and plays essential roles in reproductive development. JA-Ile production starts with polyunsaturated fatty acids esterified in plastidial membranes that are converted to OPDA, which is then transported to peroxisomes for JA formation, and finally conjugated to Ile in the cytosol to produce the bioactive hormone. While the genetic components involved in JA-Ile biosynthesis, perception and signaling have been uncovered, intracellular signaling events activating JA-Ile production and molecular mechanisms regulating biosynthetic enzyme functions have remained elusive. This review summarizes the current understanding of JA-Ile biosynthesis initiation, primarily in Arabidopsis, and highlights both recent advances and remaining challenges, with implications from long-distance signaling and emphasis on local wound responses.
