BACKGROUND AND AIMS:Plant elicitor peptides (Peps), which originate from their precursor proteins known as PROPEPs, play essential roles as signaling molecules that modulate both plant defense responses and developmental processes. METHODS:In this study, we investigated the role of PROPEP2 and its derived peptide Pep2, in regulating root hair development in Arabidopsis thaliana. Root hairs at different growth stages along the primary root and in distinct zones of the root tip were analyzed. We further examined the relationship between Pep2 and auxin signaling in regulating root hair growth. KEY RESULTS:Our findings indicate that loss of PROPEP2 function results in markedly decreased root hair number and elongation during the primary root development phase, whereas root hair formation during the embryonic root stage remains unaffected. Notably, exogenous Pep2 application rescued these defects and even induced root hair formation in non-hair-forming regions. We further demonstrated that Pep2 enhances root hair growth by stimulating localized auxin production in the root tip region. The mutants defective in auxin production (yuc1 yuc4 and wei8 tar1 tar2) failed to respond to Pep2. Furthermore, we identified the receptor-like kinases FERONIA (FER) and [Ca2+]cyt-associated protein kinase 1 (CAP1) as critical components of the Pep2 signaling pathway, with mutations in these genes impairing root hair growth and rendering plants unresponsive to Pep2. CONCLUSIONS:These results uncover a previously uncharacterized interaction between Pep2 and auxin signaling components in the regulation of root hair development, offering additional insights into the molecular control of root morphology.

This commentary spotlights landmark work from Guo et al. resolving the structure of the octameric resistosome formed by the active CCG10-nucleotide-binding leucine-rich repeat (NLR) immune receptor WAI3, which triggers sustained, multi-phasic Ca2+ influx. This fills a major knowledge gap regarding EDVID-lacking plant NLRs and provides insight into plant effector-triggered immunity.

Plants deploy sophisticated adaptive mechanisms to mitigate the detrimental effects of abiotic stresses (drought, salinity, temperature extremes, and heavy metals) and biotic stresses (pathogens and senescence) on growth and productivity. Central to these responses are transcription factors (TFs) that orchestrate stress-responsive gene networks. Among TF families, MADS-box proteins, characterized by their evolutionarily conserved DNA-binding domain, function as pivotal regulators of developmental plasticity and stress adaptation. While recent advances have clarified their roles in abiotic stress tolerance, a systematic integration of their functions in biotic stress responses has yet to be achieved. This review synthesizes current knowledge on how MADS-box TFs mediate plant adaptation to both abiotic and biotic stresses through the regulation of intricate transcriptional networks. By integrating these multifaceted insights, we advance toward a unified understanding of the molecular mechanisms by which MADS-box TFs coordinate plant responses to dual environmental challenges. Our analysis provides mechanistic insights into enhancing plant resilience through the targeted modulation of MADS-box genes and their regulatory networks. We further propose translational strategies for crop improvement, focusing on molecular breeding approaches to engineer stress-tolerant varieties that balance stress adaptation with developmental processes. This comprehensive assessment establishes MADS-box TFs as master regulators at the stress-development interface and proposes novel biotechnological avenues for sustainable agriculture.

When plants encounter biotic and abiotic stresses, they emit various volatile organic compounds to communicate with nearby plants and activate airborne defense (AD). One critical compound in this process is methyl salicylate (MeSA). Previous studies have mostly examined how stress triggers the production of MeSA at the gene level. In our study, we found that MeSA plays a key role in AD during bacterial infections and determined how plants boost MeSA production through a protein complex. Infection by Pseudomonas syringae pv. tomato DC3000 in Arabidopsis thaliana increased salicylic acid levels, leading to the formation of a ternary protein complex in the cytoplasm. This complex consists of benzoic acid/salicylic acid carboxyl methyltransferases (BSMT1), salicylic acid-binding protein 3 (SABP3), and S-adenosyl methionine synthetase 2 (MAT2). Together, they enhance MAT2's ability to produce S-adenosyl methionine (SAM), a precursor to MeSA, and boost BSMT1's capacity to synthesize MeSA. The produced MeSA then triggers AD in nearby plants and initiates systemic acquired resistance in the infected plant. Our findings clarify the MeSA production pathway during pathogen attacks and show that MeSA-mediated AD is a common defense against both insect and pathogen threats, emphasizing its potential as a potent plant immune inducer.

Crops are continually challenged by biotic stresses, including fungal, bacterial and viral pathogens and insect pests, which cause substantial yield and quality losses worldwide. WRKY transcription factors constitute a plant-specific and functionally diverse family that is central to immune regulation. Recent advances in genomic resources and multi-omics approaches have accelerated the identification and functional characterisation of WRKYs in crops. This review summarises the structural features and classification of WRKY genes and their genome-wide distribution across crop species. It also synthesises WRKY-centred regulatory modules that mediate resistance to major classes of biotic stress. In antifungal defence, WRKYs reinforce pattern- and effector-triggered immunity, modulate protein stability and reprogramme secondary metabolism. In antibacterial immunity, they link bacterial perception to cell wall remodelling and hormone and redox signalling. WRKYs also activate PR gene expression, cell wall fortification, RNA interference and programmed cell death to combat oomycete and viral pathogens and insect pests. Overall, WRKYs function as context-dependent transcriptional hubs. They integrate immune signalling with hormonal crosstalk, remodel defence gene networks, and redirect secondary metabolism, thereby shaping resistance outcomes under biotic stress. The review examines WRKY-mediated defence-growth trade-offs and explores opportunities to harness WRKY-centred networks for breeding and engineering broad-spectrum, durable disease and pest resistance. It also highlights how integrating multi-omics with precision genome editing, synthetic biology, gene-drive technologies and artificial intelligence could establish WRKYs as central molecular targets for improving crop resilience and performance.

Salicylic acid (SA) is essential for plant immunity, but excessive SA accumulation accelerates leaf senescence, necessitating tight control of its biosynthesis. Although AVRPPHB SUSCEPTIBLE3 (PBS3) is a key enzyme in SA biosynthesis, how PBS3 abundance is regulated to coordinate immunity and longevity remains unclear. Using genetic, biochemical, and physiological analyses, we show that PBS3 functions as a quantitative regulator of the immunity-longevity balance. Loss of PBS3 compromises disease resistance but delays senescence, whereas graded increases in PBS3 abundance progressively enhance pathogen-induced SA accumulation, systemic acquired resistance (SAR), and senescence severity. We further identify the E3 ubiquitin ligase PLANT U-BOX PROTEIN 13 (PUB13) as a direct regulator of PBS3. PUB13 physically associates with PBS3 and promotes its polyubiquitination and degradation through the 26S proteasome pathway. Disruption of PUB13 stabilizes PBS3, resulting in elevated SA accumulation, enhanced SAR, and accelerated leaf senescence. Time-course analyses revealed that pathogen-induced PBS3 accumulation and SA biosynthesis are transient in wild-type plants but remain elevated in pub13 mutants, indicating that PUB13 promotes the attenuation of immune-associated SA production after defense activation. Together, our findings establish the PUB13-PBS3 module as a post-translational mechanism that fine-tunes SA biosynthesis, enabling effective immunity while preventing prolonged SA accumulation and its detrimental effects on plant longevity.

While pathogen-induced local leaf stomatal closure is known to be crucial for plant immunity, whether local infection triggers stomatal closure in distant leaves has remained unknown. Recently, Liu et al. discovered that an upstream open reading frame-encoded mobile peptide and its receptor-coreceptor pair activate systemic stomatal immunity.

While plant pathogens rely on their hosts for nutrients, the specific way they take these nutrients remains unclear. Recently, Wang et al. discovered that the bacterial type III effector AvrBs2 acts as a xanthosan synthetase, facilitating the transformation of uridine 5'-diphosphate-α-D-galactose into a sugar phosphodiester known as bis-(1,6)-cyclic dimeric α-D-galactose-phosphate, or xanthosan. When xanthosan is released from the plant’s cytoplasm into the apoplastic space, Xanthomonas species absorb it via the XanT transporter and break it down with the XanP phosphodiesterase to use as a source of nutrition. Overexpression of XanP in rice blocks the nutrient supply for Xanthomonas oryzae pv. oryzicola (Xoc), making the crop resistant to bacterial leaf streak disease.

Grasping the dynamics between plants and herbivores, as well as the defenses triggered by insects, may hold the key to eco‐friendly pest management. Entomopathogenic nematodes (EPNs) have recently emerged as a promising biocontrol strategy, leading researchers to closely investigate how EPN‐infected cadavers influence plant defenses. A recent study 1 revealed notable alterations in herbivore performance and a boost in defense chemicals in maize plants treated with these infected remains. These cadavers trigger the release of volatile organic compounds from plants, which discourage the herbivorous insect Spodoptera frugiperda from feeding and laying eggs while simultaneously attracting parasitic wasps. This activation of herbivore resistance in plants treated with EPN‐infected cadavers is evident through increased levels of defense hormones, elevated enzyme activity, and the heightened expression of defense‐related genes. The research also highlighted that different EPN species cause varying effects on plant responses and herbivore behaviors, indicating a need for further investigation into the specific secondary chemicals involved. Overall, these findings enhance our understanding of complex interactions between organisms above and below the ground and point toward potential sustainable agricultural practices.

Systemin mediates systemic defense against pathogens and herbivores in solanaceous plants. However, constitutive activation of systemin-mediated defense can adversely impact plant growth. Recently, Wang et al. revealed their discovery of antiSYS, which functions as a system receptor antagonist and is instrumental in striking a balance between defense and growth.

Broad-spectrum resistance (BSR) is highly sought after for the effective management of crop diseases. However, genes suitable for developing BSR remain scarce. In this study, we demonstrate the development of BSR to wheat yellow rust (YR), powdery mildew (PM), and leaf rust (LR) diseases elicited by three biotrophic fungal pathogens using a newly defined module, namely, RFEL1-NPR3. RFEL1 is an active RING-finger E3 ubiquitin ligase identified in diploid and polyploid wheat species, which ubiquitinates and promotes the degradation of wheat NPR3 (TaNPR3), an important negative immune regulator conserved in higher plants, via the 26S proteasome system. Downregulation of TaNPR3 by either overexpressing RFEL1 or knocking out TaNPR3 confers strong resistance against four different YR races as well as the PM and LR diseases without adverse effects on wheat growth and yield traits. Notably, the enhanced disease resistance exhibited by RFEL1-overexpressing and TaNPR3-knockout lines is correlated with increased expression of defense related genes and elevated stability of NPR1, a pivotal positive regulator of plant immune signaling. Our findings underscore the importance of ubiquitination-dependent NPR3 degradation in plant immunity and advocate for the application of the RFEL1-NPR3 module in engineering BSR against biotrophic fungal pathogens in wheat and other crops.

While nucleotide-binding and leucine-rich repeat(NLR)receptors play an important role in protecting plants from pathogen infections,their practical application in disease control has faced challenges due to the swift changes in pathogens and the absence of broad and lasting resistance.Wang et al.recently engineered innovative pathogen-activated autoactive NLRs that deliver broad-spectrum plant immunity against these threats. Plant diseases pose serious threats to world food security and human health by reducing crop yield and quality.One of the most economical and eco-friendly approaches to managing plant diseases is to cultivate disease-resistant crops.Plant disease resistance can be categorized into complete resistance and partial resistance.1,2 Complete resistance is further divided into classic complete resistance with visible hypersensitive response(HR)and extreme resistance without visible HR.

Rice stands as the most significant crop in China,but it fre-quently encounters diseases that lead to an average yield loss of 10％to 30％[1].Over the past decade,the area affected by rice pests and diseases in China has ranged from 18 to 27 million hectares annually,leading to a loss of 1.3 to 2 million tons of rice[2].Iden-tifying genes that confer broad and durable disease resistance,along with elucidating the molecular mechanisms underlying plant immune activation and broad-spectrum resistance regula-tion,constitutes the fundamental theoretical foundation for breed-ing disease-resistant crops.

This commentary examines two recent papers featuring intriguing discoveries on the molecular processes and structural foundations involved in the activation and suppression of the N-requirement gene 1 (NRG1) helper nucleotide-binding leucine-rich repeat receptor.

This Commentary examines research by Wu et al. showing that β-1,3-glucan synthase-like 5 (GSL5) functions as a key gene for susceptibility to clubroot in Brassica family members by suppressing immunity regulated by jasmonic acid. Inaction of GSL5 through genome editing provides broad-spectrum resistance to clubroot.

Citrus Huanglongbing(HLB),often referred to as greening dis-ease,is a devastating bacterial disease that infects citrus trees.This disease results in blotchy mottling of leaves,premature fruit drop,twig dieback,stunted growth,lower fruit yield,and misshapen,bitter or sour fruits[1].HLB has been detected in more than 58 countries across continents including Asia,the Americas,Africa,Oceania,and the Caribbean[2].It is the leading cause of citrus decline worldwide,significantly impacting citrus production in major producing nations such as Brazil,China,and the USA[2,3].