ABSTRACT The plant root tip is highly sensitive to environmental cues and exerts sensory, chemical and movement responses. However, the microbial diversification at the root tip, and the nature of root‐selection for microbes, are poorly understood. This study investigated root exudation and microbiome colonisation in the chickpea ( Cicer arietinum L.) root tip and root base, in diverse soils. For the endosphere microbiome, deterministic effects were more important than stochastic processes in shaping the root tip microbiome, indicated by the stable endophyte composition independent of the soil microbiota background. A genotype with high secretion of benzoic acid (BA), was consistently colonised by 3 core ASV (Amplicon Sequence Variant) from the Burkholderia clade. Two of 98 isolated strains were confirmed as the culturable candidates of the core ASV, both of which were characterised by superior BA tolerance and the ability to utilise BA as a sole carbon source, demonstrated through high expression of BA degradation genes. Additionally, one IAA‐producing coloniser specifically promoted the growth of its original host genotype across different soils, but provided no consistent benefits for other genotypes. Our results reveal the mechanisms by which soil microbes interact with root exudates of a host genotype to establish colonisation.
ABSTRACT Alternaria alternata is a common pathogen responsible for leaf spots and postharvest decay in multiple crops, including sweet cherry. Coumarin, a plant‐derived compound, exhibits broad antifungal activity against plant pathogenic fungi including A. alternata . In this study, we found that coumarin significantly inhibited mycelial growth, conidiation, conidial germination, and infection of cherry tissues. Mechanistically, coumarin disrupted reactive oxygen species (ROS) homoeostasis, impaired membrane integrity, and inhibited ergosterol biosynthesis. Transcriptomic analysis revealed that coumarin dysregulated genes involved in membrane and sterol metabolism. Notably, coumarin activated the Hog1 (High osmolarity glycerol‐1) dependent stress response pathway, as evidenced by nuclear accumulation of AaHog1 and increased coumarin sensitivity of ∆ AaHog1 mutants. Furthermore, coumarin enhanced the efficacy of demethylation inhibitor (DMI) and dicarboximide (DCF) fungicides. Our findings demonstrate that coumarin acts through multiple antifungal mechanisms including HOG pathway activation, oxidative stress induction, and membrane disruption, highlighting its potential as a sustainable antifungal agent for controlling A. alternata .
ABSTRACT Plant pathogenic fungi are major drivers of disease in forest trees, often causing substantial ecological and economic damage. Ash dieback, caused by the ascomycete Hymenoscyphus fraxineus , has resulted in the widespread decline of Fraxinus excelsior populations throughout Europe. As infection is initiated in leaves containing diverse plant defensive metabolites, the ability of H. fraxineus to cope with host chemistry may determine successful host colonisation. We therefore investigated the responses of H. fraxineus to crude ash leaf extracts and individual defensive compounds. In contrast to the non‐ash associated fungi tested, H. fraxineus was not inhibited by crude methanolic leaf extracts or most plant defence compounds tested. In addition, H. fraxineus depleted ash compounds extensively from the growth medium. Consistent with these findings, untargeted metabolomics revealed extensive alterations of the ash leaf‐based medium by H. fraxineus , with 48% of detected chemical features being significantly reduced following fungal growth. Moreover, the growth of H. fraxineus was promoted by nearly all tested ash metabolites in minimal medium, indicating that these compounds can support fungal growth and may serve as carbon sources. Together, these results suggest that successful colonisation of ash tissues by H. fraxineus depends on its resistance to host defences, facilitated by its ability to deplete defensive compounds from colonised tissue.
ABSTRACT Cold stress severely restricts the geographical distribution and productivity of Camellia sinensis (tea plant). Although the plant cuticle wax serves as a critical barrier in resisting both biotic and abiotic stresses, its epigenetic regulation during cold stress remains poorly understood. Here, we show that exogenous arginine alleviates cold‐induced damage by increasing cuticle thickness, and enhancing the accumulation of very‐long‐chain fatty acids and alkanes. Transcriptome‐based weighted gene co‐expression network analysis identified CsKCS3 as a key regulator of wax biosynthesis. Virus‐induced gene silencing in tea plants and heterologous overexpression in Arabidopsis thaliana demonstrated that CsKCS3 positively regulates fatty acid biosynthesis and contributes to cold tolerance. Furthermore, the trimethylation of histone H3 at Lysine 4 (H3K4me3) is increased during arginine‐induced processes and enhances the expression of the CsSDG36 and CsKCS3 . Further, we identified that CsSDG36 encodes an H3K4 methyltransferase. Arginine treatment mitigated cold damage in CsSDG36 ‐silenced tea plants, which was associated with recovery of CsKCS3 expression. Mechanistically, CsSDG36 enhanced H3K4me3 enrichment at the promoter and exon regions of CsKCS3 , thereby activating CsKCS3 transcription. These findings reveal a CsSDG36‐H3K4me3‐ CsKCS3 regulatory module through which arginine promotes cuticular wax accumulation and cold tolerance in tea plants. These findings uncover a novel epigenetic circuitry in which exogenous arginine regulates chromatin remodeling to structurally fortify the epidermal lipid barrier, offering a vital conceptual framework for breeding climate‐resilient perennial crops.
ABSTRACT Plants in the field rarely encounter single stresses, and simultaneous stresses impose conflicting physiological demands that cannot be satisfied at once. Responses to such combinations are frequently non‐additive and cannot be predicted from single‐stress responses, a result that crosstalk models struggle to accommodate because they describe which pathways interact without specifying which prevails. This review proposes that peptide signalling functions as a control layer governing signal prioritisation. Under this hypothesis, secreted peptides act above the shared modules of cytosolic calcium, reactive oxygen species, and mitogen‐activated protein kinase cascades, and determine which competing input is permitted to dominate their behaviour. Evidence for this proposal spans several peptide families. CEP, CLE and RALF signalling illustrate systemic demand signalling, developmental stabilisation, and receptor complex reorganisation respectively, and the same logic extends to PEP, IDA and PSK signalling across immune, developmental, and drought contexts. Combined drought and nitrogen limitation, resolved through ABA and CEP, provides a worked case in which a global signal sets operating boundaries within which a local signal refines the response, supported by evidence now extending from Arabidopsis into cereals. We derive falsifiable predictions tested against hormone‐pathway negative controls and graded drought intensities rather than single treatments, which allows loss of prioritisation to be distinguished from general signalling fragility. We also identify a trade‐off constraining crop application, since enhancing peptide‐mediated nutrient foraging may reduce drought resilience. Substantial gaps remain in detecting peptide signals directly and in ranking peptide families under field conditions. Reframing plant signalling as a decision system rather than an input‐output relay offers a testable foundation for improving stress resilience and nutrient use efficiency in crop breeding.
