As a fundamental feature of plant cells, the cell wall sculpts plant architecture and governs environmental interactions. The cell wall is a dynamic matrix that exhibits both rigidity and plasticity, not only providing structural support but also serving as a critical signaling hub to regulate plant growth, development, and stress adaptation. Although long underappreciated, the signaling role of the cell wall has been brought to the forefront by recent breakthroughs, which have profoundly advanced our understanding of its importance and regulatory mechanisms. In this review, we summarize recent progress in cell wall signaling, particularly focusing on cell wall-derived signals, cell wall sensing mechanisms, and the functional roles of cell wall signaling in plant vegetative growth, reproduction, and abiotic stress responses.

Osmotic stress reduces turgor pressure, relaxes the extracellular matrix, and may generate tensile forces at the cell wall-plasma membrane interface. While animal and yeast cells employ force sensor clusters for mechanosensing, turgor-sensing mechanisms in plants remain unclear. Here, we identify FERONIA (FER) as a cell wall-anchored turgor sensor in land plants. Turgor reduction triggers the assembly of FER into largely immobile nanodomains and activates its kinase activity, processes that depend on cell wall anchoring mediated by its malectin A domain. The extracellular domain is essential and sufficient for FER nanodomain formation, thereby initiating outside-in signaling. Together, our findings suggest that FER senses mechanical perturbations at the cell wall-plasma membrane interface during turgor reduction and provide mechanistic insight into osmosensing in walled organisms.

Cell wall remodeling and adaptive responses are critical for plant salt tolerance. FERONIA (FER), a key cell wall sensor localized and activated at the plasma membrane, is central to this process. However, the molecular mechanisms governing its plasma membrane localization and activation remain elusive. Here, we found that phospholipase D α1 (PLDα1) and PLDδ physically interact with FER and that PLD-derived phosphatidic acid (PA) stabilizes FER at the plasma membrane and enhances its kinase activity. This PA-driven activation of FER promotes the phosphorylation of COMPANION OF CELLULOSE SYNTHASE1 (CC1), which in turn facilitates CC1 recycling and microtubule reassembly under salt stress. Genetic analyses uncover synergistic functions of PLD α 1 / PLD δ, FER , and CCs in regulating plant salt tolerance. Collectively, our findings reveal that PLDs and FER cooperatively govern microtubule organization under salt stress, unveiling a critical cross-talk between lipid signaling and cell wall signaling in response to stress conditions.

Reactive oxygen species (ROS) regulate plant growth, development, and responses to the environment. ROS production by the RESPIRATORY BURST OXIDASE HOMOLOG PROTEIN D (RBOHD) protein is regulated by PHYTOCHROME B (phyB), and phyB is phosphorylated by FERONIA, highlighting the possibility that these 3 proteins interact to regulate ROS levels during stress. We used immunoprecipitation and proximity labeling, followed by split-luciferase and functional validation assays, to study interactions among FERONIA, phyB, and RBOHD under excess light (EL) stress in Arabidopsis (Arabidopsis thaliana). We found that phyB, RBOHD, and FERONIA interact, that phosphorylation of phyB by FERONIA, as well as the kinase activity of FERONIA, are required for RBOHD-driven ROS production in response to EL stress, and that CYSTEINE-RICH RECEPTOR LIKE KINASE 10 (CRK10) and PLASMA MEMBRANE INTRINSIC PROTEIN 2;6 (PIP2;6) interact with RBOHD and phyB and are also required for EL-driven RBOHD ROS production. Our findings uncover a putative plasma membrane complex among FERONIA, RBOHD, CRK10, and PIP2;6 that interacts with phyB to regulate ROS production in Arabidopsis in response to stress. This complex could play a canonical role in the integration and regulation of multiple signaling pathways in plants.

Biomolecular condensates formed through phase separation have emerged as a central principle of cellular organization, enabling the dynamic regulation of gene expression, signaling, metabolism, and stress responses. While early conceptual advances in condensate biology have largely originated from animal and in vitro systems, plant cells present a unique set of biological and technical challenges, including rigid cell walls, turgor pressure, plastid autofluorescence, complex endomembrane organization, and acute environmental responsiveness. These distinctive features impede the direct transfer of existing methodologies and drive the development of heterogeneous experimental practices. In this community comment, we present a comprehensive methodological framework for studying biomolecular condensates in plants, spanning in silico prediction, in vitro reconstitution, molecular dynamics simulations, live-cell and super-resolution imaging, material property measurements, membrane-associated condensates, and synthetic condensate engineering. We highlight best practices, common pitfalls, and plant-specific considerations, emphasizing the need for orthogonal validation, quantitative interpretation, and physiological relevance. By consolidating current methodologies and articulating shared principles, this review aims to establish a foundation for rigorous, reproducible, and conceptually coherent research in condensate biology of plants and beyond, with emerging implications for crop genetic improvement and synthetic biology applications.

Plants deploy sophisticated mechanisms to fine-tune plant immunity, as constitutive activation of disease resistance is detrimental. The Arabidopsis (Arabidopsis thaliana) Raf-like kinase ENHANCED DISEASE RESISTANCE 1 (EDR1) negatively regulates defense responses; however, how EDR1 functions and its phosphorylation substrates remain elusive. Here, we show that EDR1 interacts with and phosphorylates the transcription factor MYC2 at T353/T357. MYC2 positively regulates powdery mildew resistance, and the phosphorylation of MYC2 at T353/T357 by EDR1 inhibits its ability to bind to DNA and subsequently suppresses its function in powdery mildew resistance. MYC2 is dephosphorylated by protein phosphatase 2A (PP2A) Bɑ at T353/T357, which releases EDR1-mediated inhibition during infection to promote transcription and resistance. PP2A Bɑ is activated by MITOGEN-ACTIVATED KINASE 15 (MPK15), a positive regulator of powdery mildew resistance. Consistently, the pp2a bɑ mutant displays EDR1-dependent susceptibility to powdery mildew. Taken together, these results show that the activation of MYC2 is dynamically modulated by EDR1 and PP2A Bɑ in plant immunity. These findings not only expand our understanding of the roles of EDR1 and MYC2 but also reveal a mechanism by which plants fine-tune MYC2-mediated powdery mildew resistance via a dynamic phosphorylation regulatory module.

Plain Language Summary We identified a complex between several different proteins at the plasma membrane that interacts with the light and temperature receptor protein phytochrome B to regulate reactive oxygen species formation during stress in plants. This complex could be involved in the regulation and integration of multiple abiotic and biotic signals in plants. ten ten ### Competing Interest Statement The authors have declared no competing interest. NSF, IOS-2414183; IOS-2110017, IOS-2343815

Leucine-rich repeat extensin (LRX) 3/4/5 and FERONIA (FER) jointly regulate plant salt tolerance, but the mechanisms by which LRX3/4/5 modulate FER activity in response to salt stress remain largely unclear. Here, we found that lrx345 mutations reduce FER kinase activity, which explains the phenotypic similarity between lrx345 and fer-4. Immunoprecipitation-mass spectrometry (IP-MS) analysis reveals a physical interaction between FER and protein phosphatase 2A (PP2A), with PP2A directly dephosphorylating FER. Disruption of PP2A restores FER kinase activity and salt hypersensitivity in the lrx345 mutant, establishing PP2A as a key negative regulator of FER kinase activity. Conversely, FER inhibits PP2A phosphatase activity through phosphorylation, forming a dynamic feedback loop. Further mechanistic studies show that FER and PP2A coordinately regulate plant salt tolerance by controlling auxin transport via the modulation of PIN3 phosphorylation. Collectively, our work unveils an antagonistic kinase-phosphatase pair that fine-tunes phosphorylation-dependent signaling to optimize plant adaptation to salt stress.

Seed dormancy and germination are crucial processes affecting the propagation and survival of plant populations. These phenomena are precisely regulated through a complex interplay between internal signals, such as plant hormones and environmental cues including light, temperature, moisture, and nutrient availability. Dormancy release and germination initiation are distinct, yet closely associated, processes involving complex transcriptional, translational, and epigenetic changes mediated by intricate regulatory mechanisms. This review comprehensively summarizes the complex regulatory networks governing seed dormancy and germination across different plant species. By integrating physiological, genetic, and molecular biology perspectives, the latest advances in the research on mechanisms regulating seed dormancy and germination are discussed, providing valuable insights for improving seed quality through biotechnology-based breeding strategies and establishing a solid foundation for future research in this field.

Seed germination is the initial step of the whole life cycle for an individual plant, and thus it needs to be tightly controlled to avoid plant growth under unfavorable conditions. Here, we report that FERONIA (FER), a receptor-like kinase, controls early seed germination under ABA conditions. FER interacts with and phosphorylates cytosolic ABA receptor kinase 1 (CARK1) protein, a receptor-like cytoplasmic kinase (RLCK) that modulates ABA signaling. In both the fer-4 and cark1 mutants, ABA-triggered SNF1-related protein kinase 2 (SnRK2) activation and ABI5 protein accumulation are attenuated. FER phosphorylates the Ser233 and Thr234 residues of CARK1, and the CARK1 protein with the substitutions of these two residues with Ala exhibits a reduced kinase activity and fails to rescue the increased seed germination rate of the cark1 mutant under ABA conditions. Collectively, our study not only uncovers an RLCK protein that functions downstream of FER but also provides a mechanistic insight into ABA-mediated early seed germination regulation by the FER-CARK1 module.

Plant pathogens manipulate host development, facilitating colonization and proliferation. Ralstonia solanacearum is a soil -borne bacterial pathogen that penetrates roots and colonizes plants through the vascular system, causing wilting and death. Here, we find that RipAC, an effector protein from R. solanacearum , alters root development in Arabidopsis , promoting the formation of lateral roots and root hairs. RipAC interacts with CELLULOSE SYNTHASE (CESA)-INTERACTIVE PROTEIN 1 (CSI1), which regulates the activity of CESA complexes at the plasma membrane. RipAC disrupts CESA-CSI1 interaction, leading to a reduction in cellulose content, root developmental alterations, and a promotion of bacterial pathogenicity. We find that CSI1 also associates with the receptor kinase FERONIA, forming a complex that negatively regulates immunity in roots; this interaction, however, is not affected by RipAC. Our work reveals a bacterial virulence strategy that selectively affects the activities of a host target, promoting anatomical alterations that facilitate infection without causing activation of immunity.

Drought tolerance is a complex trait in soybean that is controlled by polygenetic quantitative trait loci (QTLs). In this study, wilting score, days-to-wilting, leaf relative water content, and leaf relative conductivity were used to identify QTLs associated with drought tolerance in recombinant inbred lines derived from a cross between a drought-sensitive variety, Lin, and a drought-tolerant variety, Meng. A total of 33 drought-tolerance QTLs were detected. Of these 17 were major QTLs. In addition, 15 were novel drought-tolerance QTLs. The most predominant QTL was on chromosome 11. This was detected in at least three environments. The overlapped mapping interval of the four measured traits was 0.2 cM in genetic distance (about 220 kb in physical length). Glyma.11g143500 (designated as GmUAA6), which encodes a UDP-N-acetylglucosamine transporter, was identified as the most likely candidate gene. The allele of GmUAA6 from Lin (GmUAA6Lin) was associated with improved soybean drought tolerance. Overexpression of GmUAA6Lin in Arabidopsis and soybean hairy roots enhanced drought tolerance. Furthermore, a 3-bp insertion/deletion (InDel) in the coding sequence of GmUAA6 explained up to 49.9% of the phenotypic variation in drought tolerance-related traits, suggesting that this InDel might be used in future marker-assisted selection of drought-tolerant lines in soybean breeding programs.

Cell wall remodeling is important for plants to adapt to environmental stress. Under salt stress, cortical microtubules undergo a depolymerization-reassembly process to promote the biosynthesis of stress-adaptive cellulose, but the regulatory mechanisms underlying this process are still largely unknown. In this study, we reveal that FERONIA (FER), a potential cell wall sensor, interacts with COMPANION OF CELLULOSE SYNTHASE1 (CC1) and its closest homolog, CC2, two proteins that are required for cortical microtubule reassembly under salt stress. Biochemical data indicate that FER phosphorylates CC1 on multiple residues in its second and third hydrophobic microtubule-binding regions and that these phosphorylations modulate CC1 trafficking and affect the ability of CC1 to engage with microtubules. Furthermore, CC1 phosphorylation level is altered upon exposure to salt stress, which coincides with the changes of microtubule organization. Together, our study outlines an important intracellular mechanism that maintains microtubule arrays during salt exposure in plant cells.

Photorespiration is an energetically costly metabolic pathway in plants that responds to environmental stresses. The molecular basis of the regulation of the photorespiratory cycle under stress conditions remains unclear. Here, we discovered that FERONIA (FER) regulates photorespiratory flow under salt stress in Arabidopsis (Arabidopsis thaliana). FER mutation results in hypersensitivity to salt stress, but disruption of ferredoxin-dependent glutamate synthase 1 (GLU1), an enzyme that participates in the photorespiratory pathway by producing glutamate, greatly suppresses fer-4 hypersensitivity to salt stress primarily due to reduced glycine yield. In contrast, disrupting mitochondrial serine hydroxymethyltransferase1 (SHM1), which is supposed to increase glycine levels by hampering the conversion of glycine to serine in the photorespiratory cycle, aggravates fer-4 hypersensitivity to salt stress. Biochemical data show that FER interacts with and phosphorylates SHM1, and this phosphorylation modulates SHM1 stability. Additionally, the production of proline and its intermediate △1-pyrroline-5-carboxylate (P5C), which are both synthesized from glutamate, also contributes to fer-4 hypersensitivity to salt stress. In conclusion, this study elucidates the functional mechanism of FER in regulating salt tolerance by modulating photorespiratory flux, which greatly broadens our understanding of how plants adapt to high salinity.

Generation of crops with low phytic acid (myo-inositol-1,2,3,4,5,6-hexakisphosphate (InsP6)) is an important breeding direction, but such plants often display less desirable agronomic traits. In this study, through ethyl methanesulfonate-mediated mutagenesis, we found that inositol 1,3,4-trisphosphate 5/6-kinase 4 (ITPK4), which is essential for producing InsP6, is a critical regulator of salt tolerance in Arabidopsis. Loss of function of ITPK4 gene leads to reduced root elongation under salt stress, which is primarily because of decreased root meristem length and reduced meristematic cell number. The itpk4 mutation also results in increased root hair density and increased accumulation of reactive oxygen species during salt exposure. RNA sequencing assay reveals that several auxin-responsive genes are down-regulated in the itpk4-1 mutant compared to the wild-type. Consistently, the itpk4-1 mutant exhibits a reduced auxin level in the root tip and displays compromised gravity response, indicating that ITPK4 is involved in the regulation of the auxin signaling pathway. Through suppressor screening, it was found that mutation of Multidrug Resistance Protein 5 (MRP5)5 gene, which encodes an ATP-binding cassette (ABC) transporter required for transporting InsP6 from the cytoplasm into the vacuole, fully rescues the salt hypersensitivity of the itpk4-1 mutant, but in the itpk4-1 mrp5 double mutant, InsP6 remains at a very low level. These results imply that InsP6 homeostasis rather than its overall amount is beneficial for stress tolerance in plants. Collectively, this study uncovers a pair of gene mutations that confer low InsP6 content without impacting stress tolerance, which offers a new strategy for creating "low-phytate" crops.

Identification of environmental stress sensors is one of the most important research topics in plant abiotic stress research. Traditional strategies to identify stress sensors or early signaling components based on the cell membrane as a primary site of sensing and calcium signal as a second messenger have had only limited successes. Therefore, the current theoretical framework underlying stress sensing in plants should be reconsidered and additional mechanisms need to be introduced. Recently, accumulating evidence has emerged to suggest that liquid-liquid phase separation (LLPS) is a major mechanism for environmental stress sensing and response in plants. In this review, we briefly introduce LLPS regarding its concept, compositions, and dynamics, and then summarize recent progress of LLPS research in plants, emphasizing the contribution of LLPS to the sensing of various environmental stresses, such as dehydration, osmotic stress, and low and high temperatures. Finally, we propose strategies to identify key proteins that sense and respond to environmental stimuli on the basis of LLPS, and discuss the research directions of LLPS in plant abiotic stress responses and its potential application in enhancing stress tolerance in crops.

Cell wall not only supports and protects plant cells,but also serves as the first barrier for plants to resist environmental stresses.As one of the major abiotic stresses that restrict agricultural production,salt stress can cause the alteration of cell wall composition and structure,and these changes can be perceived by cell wall integrity sensors,such as CrRLK1Ls,LRXs,and WAKs,to activate intracellular salt stress responses.In the cell interior,salt stress-induced influx of Ca2+ and activation of phytohormone signaling promote the expressions of genes that are associated with cell wall biosynthesis and modification,which in turn facilitate the maintenance of cell wall integrity and improve the adaptation of plants to high salinity.In this review,the main components of primary cell wall polysaccharides and their cross-linking with each other are summarized.The impact of salt stress on cell wall polysaccharides,and the molecular mechanisms by which plants perceive and maintain cell wall integrity under salt stress,are also elucidated.Finally,the scientific questions that need to be further addressed in the research field of cell wall integrity under salt stress are discussed.

Salt stress simultaneously causes ionic toxicity, osmotic stress, and oxidative stress, which directly impact plant growth and development. Plants have developed numerous strategies to adapt to saline environments. Whereas some of these strategies have been investigated and exploited for crop improvement, much remains to be understood, including how salt stress is perceived by plants and how plants coordinate effective responses to the stress. It is, however, clear that the plant cell wall is the first contact point between external salt and the plant. In this context, significant advances in our understanding of halotropism, cell wall synthesis, and integrity surveillance, as well as salt-related cytoskeletal rearrangements, have been achieved. Indeed, molecular mechanisms underpinning some of these processes have recently been elucidated. In this review, we aim to provide insights into how plants respond and adapt to salt stress, with a special focus on primary cell wall biology in the model plant Arabidopsis thaliana.

Phosphorylation modification is required for the modulation of phytochrome B (phyB) thermal reversion, but the kinase(s) that phosphorylate(s) phyB and the biological significance of the phosphorylation are still unknown. Here we report that FERONIA (FER) phosphorylates phyB to regulate plant growth and salt tolerance, and the phosphorylation not only regulates dark-triggered photobody dissociation but also modulates phyB protein abundance in the nucleus. Further analysis indicates that phosphorylation of phyB by FER is sufficient to accelerate the conversion of phyB from the active form (Pfr) to the inactive form (Pr). Under salt stress, FER kinase activity is inhibited, leading to delayed photobody dissociation and increased phyB protein abundance in the nucleus. Our data also show that phyB mutation or overexpression of PIF5 attenuates growth inhibition and promotes plant survival under salt stress. Together, our study not only reveals a kinase that controls phyB turnover via a signature of phosphorylation, but also provides mechanistic insights into the role of the FER-phyB module in coordinating plant growth and stress tolerance.

Protochlorophyllide oxidoreductase (POR) plays a key role in catalyzing the light-dependent reduction of protochlorophyllide (Pchlide) to chlorophyllide (Chlide), and thus promotes the transit from etiolated seedlings to green plants. In this study, by exploring ethyl methanesulfonate (EMS)-mediated mutagenesis in Chenopodium quinoa NL-6 variety, we identified a mutant nl6-35 that displays faded green leaf and reduced chlorophyll (Chl) and carotenoid contents. Bulk segregant analysis (BSA) revealed that a mutation in CqPORB gene is genetically associated with the faded green leaf of the nl6-35 mutant. Further study indicates that the nl6-35 mutant exhibits abnormal grana stacks and compromised conversion of Pchlide to Chlide upon illumination, suggesting the important role of CqPORB in producing photoactive Pchlide. Totally three CqPOR isoforms, including CqPORA, CqPORA-like, and CqPORB are identified in NL-6 variety. Transcriptional analysis shows that the expression of all these three CqPOR isoforms is regulated in light- and development-dependent manners, and in mature quinoa plants only CqPORB isoform is predominantly expressed. Subcellular localization analysis indicates that CqPORB is exclusively localized in chloroplast. Together, our study elucidates the important role of CqPORB in the regulation of Chl biosynthesis and chloroplast development in quinoa.