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Pathogen attack sequentially confers pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) after sensing of pathogen patterns and effectors by plant immune receptors, respectively. Reactive oxygen species (ROS) play pivotal roles in PTI and ETI as signaling molecules. Nicotiana benthamiana RBOHB, an NADPH oxidase, is responsible for both the transient PTI ROS burst and the robust ETI ROS burst. Here, we show that RBOHB transactivation mediated by MAPK contributes to R3a/AVR3a-triggered ETI (AVR3a-ETI) ROS burst. RBOHB is markedly induced during the ETI and INF1-triggered PTI (INF1-PTI), but not flg22-tiggered PTI (flg22-PTI).We found that the RBOHB promoter contains a functionalW-box in the R3a/AVR3a and INF1 signalresponsive cis-element. Ectopic expression of four phospho-mimicking mutants of WRKY transcription factors, which are MAPK substrates, induced RBOHB, and yeast one-hybrid analysis indicated that these mutants bind to the cis-element. Chromatin immunoprecipitation assays indicated direct binding of the WRKY to the cis-element in plants. Silencing of multiple WRKY genes compromised the upregulation of RBOHB, resulting in impairment of AVR3a-ETI and INF1-PTI ROS bursts, but not the flg22-PTI ROS burst. These results suggest that the MAPK-WRKY pathway is required for AVR3a-ETI and INF1-PTI ROS bursts by activation of RBOHB.

Crop leaves in full sunlight dissipate damaging excess absorbed light energy as heat. When sunlit leaves are shaded by clouds or other leaves, this protective dissipation continues for many minutes and reduces photosynthesis. Calculations have shown that this could cost field crops up to 20% of their potential yield. Here, we describe the bioengineering of an accelerated response to natural shading events in Nicotiana (tobacco), resulting in increased leaf carbon dioxide uptake and plant dry matter productivity by about 15% in fluctuating light. Because the photoprotective mechanism that has been altered is common to all flowering plants and crops, the findings provide proof of concept for a route to obtaining a sustainable increase in productivity for food crops and a much-needed yield jump.

Plants produce receptors that recognize fragments of microbial flagellin, thus monitoring for infection by bacteria. Buscaill et al. studied how a flagellin fragment is made accessible for recognition by host glycosidases, which degrade the glycosylations shielding the peptide that triggers the immune response. The pathogen, in turn, evades detection by altering flagellin glycosylation and inhibiting the host glycosidase. This aspect of plant defense against infection plays out in the apoplast, the extracellular space within plant tissues. Science , this issue p. eaav0748 Microbial pathogen and host defenses compete through glycosylation of a flagellin fragment. Plants and animals recognize conserved flagellin fragments as a signature of bacterial invasion. These immunogenic elicitor peptides are embedded in the flagellin polymer and require hydrolytic release before they can activate cell surface receptors. Although much of flagellin signaling is understood, little is known about the release of immunogenic fragments. We discovered that plant-secreted β-galactosidase 1 (BGAL1) of Nicotiana benthamiana promotes hydrolytic elicitor release and acts in immunity against pathogenic Pseudomonas syringae strains only when they carry a terminal modified viosamine (mVio) in the flagellin O -glycan. In counter defense, P. syringae pathovars evade host immunity by using BGAL1-resistant O -glycans or by producing a BGAL1 inhibitor. Polymorphic glycans on flagella are common to plant and animal pathogenic bacteria and represent an important determinant of host immunity to bacterial pathogens.

Pathogen-associated molecular patterns (PAMPs) are conserved molecules that are crucial for normal life cycle of microorganisms. However, the diversity of microbial PAMPs is little known. During screening of cell-death-inducing factors from the necrotrophic fungus Valsa mali, we identified a novel PAMP VmE02 that is widely spread in oomycetes and fungi. Agrobacterium tumefaciens-mediated transient expression or infiltration of recombinant protein produced by Escherichia coli was performed to assay elicitor activity of the proteins tested. Virus-induced gene silencing in Nicotiana benthamiana was used to determine the components involved in VmE02-triggered cell death. The role of VmE02 in virulence and conidiation of V. mali were characterized by gene deletion and complementation. We found that VmE02, together with some of its homologues from both oomycete and fungal species, exhibited cell-death-inducing activity in N. benthamiana. VmE02-triggered cell death was shown to be dependent on BRI1-ASSOCIATED KINASE-1, SUPPRESSOR OF BIR1- 1, HSP90 and SGT1 in N. benthamiana. Deletion of VmE02 in V. mali greatly attenuated pathogen conidiation but not virulence, and treatment of N. benthamiana with VmE02 enhances plant resistance to Sclerotinia sclerotiorum and Phytophthora capsici. We conclude that VmE02 is a novel cross-kingdom PAMP produced by several fungi and oomycetes.

Aphids transmit viruses and are destructive crop pests 1 . Plants that have been attacked by aphids release volatile compounds to elicit airborne defence (AD) in neighbouring plants 2 – 5 . However, the mechanism underlying AD is unclear. Here we reveal that methyl-salicylate (MeSA), salicylic acid-binding protein-2 (SABP2), the transcription factor NAC2 and salicylic acid-carboxylmethyltransferase-1 (SAMT1) form a signalling circuit to mediate AD against aphids and viruses. Airborne MeSA is perceived and converted into salicylic acid by SABP2 in neighbouring plants. Salicylic acid then causes a signal transduction cascade to activate the NAC2–SAMT1 module for MeSA biosynthesis to induce plant anti-aphid immunity and reduce virus transmission. To counteract this, some aphid-transmitted viruses encode helicase-containing proteins to suppress AD by interacting with NAC2 to subcellularly relocalize and destabilize NAC2. As a consequence, plants become less repellent to aphids, and more suitable for aphid survival, infestation and viral transmission. Our findings uncover the mechanistic basis of AD and an aphid–virus co-evolutionary mutualism, demonstrating AD as a potential bioinspired strategy to control aphids and viruses. Aphid-transmitted viruses encode proteins that suppress the plant airborne defence response—which is triggered by volatile chemicals released by neighbouring plants after aphid attack—and the plants consequently become less repellent to aphids and more suitable for aphid survival, infestation and viral transmission.

The Calvin cycle is the initial pathway of photosynthetic carbon fixation, and several of its reaction steps are suggested to exert rate-limiting influence on the growth of higher plants. Plastid fructose 1,6-bisphosphate aldolase (aldolase, EC 4.1.2.13) is one of the nonregulated enzymes comprising the Calvin cycle and is predicted to have the potential to control photosynthetic carbon flux through the cycle. In order to investigate the effect of overexpression of aldolase, this study generated transgenic tobacco (Nicotiana tabacumL. cv Xanthi) expressingArabidopsisplastid aldolase. Resultant transgenic plants with 1.4–1.9-fold higher aldolase activities than those of wild-type plants showed enhanced growth, culminating in increased biomass, particularly under high CO₂ concentration (700 ppm) where the increase reached 2.2-fold relative to wild-type plants. This increase was associated with a 1.5-fold elevation of photosynthetic CO₂ fixation in the transgenic plants. The increased plastid aldolase resulted in a decrease in 3-phosphoglycerate and an increase in ribulose 1,5-bisphosphate and its immediate precursors in the Calvin cycle, but no significant changes in the activities of ribulose 1,5-bisphosphate carboxylase/oxygenase (Rubisco) or other major enzymes of carbon assimilation. Taken together, these results suggest that aldolase overexpression stimulates ribulose 1,5-bisphosphate regeneration and promotes CO₂ fixation. It was concluded that increased photosynthetic rate was responsible for enhanced growth and biomass yields of aldolase-overexpressing plants.

Background Abscisic acid (ABA) is an important phytohormone for plant growth, development and responding to stresses such as drought, salinity, and pathogen infection. Pyrabactin Resistance 1 (PYR1)/PYR1-Like (PYL)/Regulatory Component of ABA Receptor (RCAR) (hereafter referred to as PYLs) has been identified as the ABA receptors. The PYL family members have been well studied in many plants. However, the members of PYL family have not been systematically identified at genome level in cultivated tobacco ( Nicotiana tabacum ) and its two ancestors. In this study, the phylogenic relationships, chromosomal distribution, gene structures, conserved motifs/regions, and expression profiles of NtPYL s were analyzed. Results We identified 29, 11, 16 PYL s in the genomes of allotetraploid N. tabacum , and its two diploid ancestors N. tomentosiformis and N. sylvestris , respectively. The phylogenetic analysis revealed that NtPYLs can be divided into three subfamilies, and each NtPYL has one counterpart in N. sylvestris or N. tomentosiformis . Based on microarray analysis of NtPYL transcripts, four NtPYL s (from subfamily II, III), and five NtPYL s (from subfamily I) are highlighted as potential candidates for further functional characterization in N. tabacum seed development, response to ABA, and germination, and resistance to abiotic stresses, respectively. Interestingly, the expression profiles of members in the same NtPYL subfamily showed somehow similar patterns in tissues at different developmental stages and in leaves of seedlings under drought stress, suggesting particular NtPYLs might have multiple functions in both plant development and drought stress response. Conclusions NtPYL s are highlighted for important functions in seed development, germination and response to ABA, and particular in drought tolerance. This work will not only shed light on the PYL family in tobacco, but also provides some valuable information for functional characterization of ABA receptors in N. tabacum .

Microplastics derived from biodegradable PBAT film, widely used in agriculture, pose ecological and biological hazards. This study explores how T4 mitigates this microplastic-induced stress in . Using five experimental setup-control (CK), low/high-dose aged microplastics (MP80/MP320), and their co-treatments with T4 (MP80+T4/MP320+T4), multi-omics analyses reveal the microplastic stress-alleviating mechanisms of T4. Aged microplastics significantly inhibit plant growth, promote reactive oxygen species (ROS) and malondialdehyde (MDA) accumulation, and disrupt metabolic homeostasis. Conversely, T4 activates the plant antioxidant defense system, reducing ROS/MDA levels and upregulating superoxide dismutase (SOD)/peroxidase (POD) activities, and promotes biomass. Transcriptomic analysis shows T4 reverses gene expression patterns disrupted by microplastics, particularly in DNA replication and pentose-glucuronic acid pathways. Metagenomic sequencing indicates T4 restores soil microbial diversity, increases the abundance of and , downregulates antibiotic resistance genes (e.g., , ), and upregulates carbohydrate-active enzymes (CAZys), thereby enhancing carbon metabolism. In conclusion, T4 alleviates microplastic stress through a tripartite mechanism: activating plant stress-response gene networks, reshaping soil microbial communities, and modulating functional gene expression, offering a promising bioremediation strategy.

Asparagine synthetase B (AS-B) is essential for nitrogen metabolism, but its broader physiological functions remain poorly understood. Here we show that the evolutionarily conserved Nicotiana benthamiana NbAS-B confers expression-dependent antiviral resistance and promotes plant growth. Multi-omics analyses indicate that NbAS-B-mediated antiviral immunity relies on glutamate-induced activation of Ca²⁺ signaling through the receptor GLR3.3, whereas its growth-promoting effect results from photosynthetic reprogramming. Building on these insights, we develop polyglutamate-loaded chitosan nanogels (PGANPs) to artificially manipulate this pathway. These nanogels efficiently enter plant tissues and enable sustained in situ release of glutamate, thereby mimicking and amplifying NbAS-B signaling outputs. PGANPs provide long-lasting systemic antiviral immunity while concurrently enhancing plant growth, without incurring metabolic costs. Our work identifies NbAS-B as a dual-function regulator linking metabolic status to immune activation and establishes PGANPs as an eco-friendly, controllable, and durable nanobiotechnology for managing viral diseases in crops. Controlling plant metabolism to improve growth and disease resistance has huge potential. Here, the authors find a conserved pathway which promotes antiviral resistance and promotes plant growth and develop polyglutamate-loaded chitosan nanogels to manipulate this pathway.

In pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI), plant cell surface receptors sense potential microbial pathogens by recognizing elicitors called PAMPs. Although diverse PAMPs trigger PTI through distinct receptors, the resulting intracellular responses overlap extensively. Despite this, a common component(s) linking signal perception with transduction remains unknown. In this study, we identify SOMATIC EMBRYOGENESIS RECEPTOR KINASE (SERK)3/brassinosteroid-associated kinase (BAK)1, a receptor-like kinase previously implicated in hormone signaling, as a component of plant PTI. In Arabidopsis thaliana, AtSERK3/BAK1 rapidly enters an elicitor-dependent complex with FLAGELLIN SENSING 2 (FLS2), the receptor for the bacterial PAMP flagellin and its peptide derivative flg22. In the absence of AtSERK3/BAK1, early flg22-dependent responses are greatly reduced in both A. thaliana and Nicotiana benthamiana. Furthermore, N. benthamiana Serk3/Bak1 is required for full responses to unrelated PAMPs and, importantly, for restriction of bacterial and oomycete infections. Thus, SERK3/BAK1 appears to integrate diverse perception events into downstream PAMP responses, leading to immunity against a range of invading microbes.