Molecular Plant-microbe Interactions最新文献

Plant-parasitic nematodes (PPNs) are a serious threat to global food security, with estimated annual losses exceeding $173 billion. Beyond their direct damage, interactions between PPNs and other phytopathogens can lead to synergistic relationships, referred to as disease complexes, which result in more severe symptoms than either pathogen alone. Disease complexes have been documented across diverse PPN species with distinct lifestyles, including migratory ectoparasites, migratory endoparasites, and sedentary endoparasites, and have been shown to involve partners spanning viruses, bacteria, oomycetes, and fungi. In this review, we discuss specific aspects of PPN life cycles that may facilitate disease complex formation. Nematode-induced wounding may provide entry points or release exudate signals that promote secondary pathogen infection. Nutrient-rich feeding sites established by endoparasitic nematodes may support proliferation of secondary parasites. Furthermore, certain PPN families can vector pathogens such as viruses directly into the plant via their stylet or by carrying bacteria on the cuticle surface. Finally, PPNs can suppress or evade host immune responses, thereby increasing plant susceptibility to other microbial pathogens. Elucidating the molecular mechanisms underlying these interactions will improve our understanding of disease complexes associated with PPN infection and may inform the development of novel management strategies to mitigate their impact on agricultural systems. [Formula: see text] The author(s) have dedicated the work to the public domain under the Creative Commons CC0 "No Rights Reserved" license by waiving all of his or her rights to the work worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law, 2026.

Agroathelia rolfsii causes stem rot in multiple crops, survives as sclerotia in the absence of host plants, and remains a difficult-to-manage pathogen globally. Although Trichoderma species offer a sustainable biocontrol solution, their dual roles as antagonists and plant biostimulants present a complex trade-off under stress conditions that remains underexplored. This study analyzed the pathogen suppression and plant growth promotion induced by Trichoderma virens DM5 in the context of tomato protection against A. rolfsii. Using a combination of phenotypic assays and transcriptomic analyses, we observed that T. virens DM5 suppressed A. rolfsii via both mycoparasitism and antibiosis, producing antifungal compounds that inhibited pathogen growth. Simultaneously, it enhanced host vigor by increasing seed germination by 54.5% and plant survival rates by 70% under pathogen pressure. Molecular analyses revealed that plants treated with T. virens DM5 exhibited rapid early activation of defense-associated pathways, including MAPK signaling, MYB transcription factors, and amino sugar metabolism within 24 h post inoculation, followed by attenuation of prolonged defense responses. These responses reduced the need for prolonged immune activation, suggesting an energy-saving strategy, allowing the plant to allocate resources toward development and survival. These findings highlight the multifaceted role of T. virens DM5 in sustaining tomato growth and disease suppression under A. rolfsii-conducive conditions. By combining direct antagonism with strategic modulation of plant defense, T. virens facilitates an optimized biocontrol-biostimulant trade-off. Understanding this interplay is critical for enhancing the efficacy of Trichoderma-based applications in climate-smart, sustainable agriculture. [Formula: see text] Copyright © 2025 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Induced systemic resistance (ISR) is an essential strategy in biological control. Previous research has shown that Bacillus cereus AR156 can trigger ISR to defend against multiple pathogens, though the underlying mechanisms may vary depending on the pathogen. However, the specific mechanism by which AR156 induces systemic resistance against Ralstonia solanacearum in tomatoes remains unclear. In this study, we focused on WRKY group I transcription factors and identified WRKY4, which is downregulated by AR156 induction. Further analysis confirmed that WRKY4 functions as a negative regulator in AR156-ISR against tomato bacterial wilt. Experimental results demonstrated that WRKY4 is localized in the nucleus and exhibits transcriptional regulatory activity. Subsequent screening revealed that WRKY4 directly targets the promoter region of the SSL3 (Strictosidine Synthase-Like) gene, which encodes a key synthase for metabolic precursors, and consequently suppresses its expression. Finally, we confirmed that WRKY4 negatively regulates SSL3 expression, contributing to AR156-ISR against tomato bacterial wilt as a key negative regulator. Our research enriches our understanding of the ISR network and provides a theoretical foundation for the biological control of diseases. [Formula: see text] The author(s) have dedicated the work to the public domain under the Creative Commons CC0 "No Rights Reserved" license by waiving all of his or her rights to the work worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law, 2026.

The filamentous fungus Elsinoë arachidis is a major foliar pathogen responsible for peanut scab, which is a significant disease affecting commercial peanut cultivation. Elsinochrome (ESC), produced by numerous phytopathogenic Elsinoë species, is a non-host-selective polyketide phytotoxin with strong photosensitive activity and plays a crucial role in pathogenesis on host plants. In E. arachidis, a dual-domain enzyme encoded by the gene ESCB3, containing both O-methyltransferase and a FAD-dependent monooxygenase domain, has been identified. To elucidate the role of ESCB3, the biological function, expression pattern of the ESC biosynthesis gene cluster, and associated metabolomics analyses were investigated in the present study. An ESCB3 deletion mutant (ΔESCB3) was created by targeted gene disruption. Notably, ESC production was completely blocked in the ΔESCB3 mutant, and the expression of ESC biosynthetic genes, except for the polyketide synthase gene ESCB1, was significantly downregulated. Additionally, the ΔESCB3 exhibited heightened sensitivity to multiple stress tolerance compared with the wild type, especially oxidative stress/H₂O₂, highlighting the crucial role of ESCB3 in growth, development, and ESC biosynthesis in E. arachidis. Pathogenicity assays revealed a significant reduction in the pathogenicity of the ΔESCB3 mutant, suggesting a possible correlation with the suppressed biosynthesis of ESC. Metabolomic analyses further confirmed that ESCB3 is indispensable for the ESC biosynthetic process and acts as a key regulatory factor. Collectively, the results of this study provide significant insights into the molecular mechanisms governing ESCB3-mediated virulence and ESC production in E. arachidis, offering potential targets for disease control strategies in peanut scab. [Formula: see text] Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Plants are constantly exposed to diverse pathogens and have evolved sophisticated defense mechanisms to detect and respond to microbial threats. Pathogen recognition is often mediated by pathogen-associated molecular patterns (PAMPs), such as cell wall components or secreted molecules. Quorum-sensing molecules, secreted by bacteria to regulate virulence factors, are an emerging class of PAMPs that plants can detect as signs of infection. One such molecule, diffusible signal factor (DSF), is secreted by Xanthomonas plant pathogens. Previous studies have shown that DSF induces immune responses in plants such as Arabidopsis and rice. However, the plant mechanisms involved in DSF perception and immune response remain poorly understood. In this study, we performed transcriptome analysis to investigate the molecular players involved in DSF-induced immunity in Arabidopsis. Our findings identified key molecules, including WRKY66, PEPR2, and WAK_PK, as players in DSF-mediated immune responses. However, none of these molecules appears to directly recognize DSF, as mutants still activate DSF-induced MAP kinase signaling. This suggests that additional unidentified receptors or signaling pathways may play a role in DSF perception. Our study elaborates the downstream events of DSF recognition as a PAMP and contributes to the growing body of knowledge on plant immune signaling. [Formula: see text] Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Plant resistance (R) and pathogen avirulence (Avr) gene interactions are central to pathogen recognition and disease resistance in crops. Functional characterization of recognized Avr effectors of Puccinia striiformis f. sp. tritici (Pst) lags other key fungal pathogens of wheat. Here, we used a wheat protoplast-based screen to identify Avr/R interactions via the proxy of effector-induced defense responses in a set of diverse wheat cultivars. We identified an Avr candidate, termed AvrPstB48, that triggers defense responses in 16 out of 24 cultivars tested. AvrPstB48 is hemizygous, and the Pst genome carries four divergent paralogs within a gene cluster. Analysis of these paralogs revealed partial redundancy in their ability to activate wheat defenses and enabled us to identify a single amino acid in AvrPstB48 that is necessary but not sufficient for defense activation. Notably, the activation of defense signaling by AvrPstB48 in protoplasts did not directly correlate with disease outcomes. Whole-plant infection assays revealed that some cultivars that exhibited strong defense activation in the protoplast assay are susceptible to the Pst isolate Pst104E137A, from which AvrPstB48 is derived. Comparison of the infection dynamics of two wheat cultivars that differ in their AvrPstB48 recognition capacity revealed a delay in disease progression in the recognizing cultivar Avocet S compared with the non-recognizing cultivar Morocco. Although correlative only, our observations, combined with other recent reports, support a "recognize-then-suppress" model of plant-pathogen interaction in which disease outcomes are driven not only by simple Avr/R interactions but also by pathogen effectors that suppress defense signaling downstream of effector recognition. [Formula: see text] Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY 4.0 International license.

All pathogens must sense that they have arrived at their host. This is a necessary part of infection in order to effect the changes in pathogen biology required to progress through their life cycle. How the information that they have arrived is transmitted, and what molecules/media convey the information, is poorly understood. Here, we review recent literature and provide speculation as to how this might happen, by analogy to the five human senses. Our criteria center on natural selection: we consider host-derived signals-in the broadest sense-to be those that carry some information and that can be detected by the pathogen, in principle. For each, we identify supporting literature and speculate on areas of possible expansion. We conclude, on the one hand, that there is a diversity of understudied but compelling signals, but, on the other hand, that not all signals are equal. The magnitude of the response is likely a function of the fidelity of the signal/detection. Although knowledge is currently incomplete, the prospect of understanding perception of arrival at the host may allow us to perturb pathogen perception of the host and thereby thwart this early and fundamental step in pathogen development. [Formula: see text] Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY 4.0 International license.

Invasive, lethal tree diseases continue to have devastating effects on forest ecology, commercial timber production, the horticultural trade, and agriculture production. Laurel wilt, caused by the recently introduced fungus Harringtonia lauricola, is one such lethal disease threatening both native ecosystems and avocado production. Previous transcriptomic analyses determined that a massive upregulation of pathogen genes involved in the uptake and metabolism of sulfur compounds occurs during host colonization. The creation of a loss-of-function mutant for pathogen-encoded HlCys3, a bZIP transcriptional regulator of alternative sulfur utilization, abolished colonization and disease. This phenotype was complemented genetically and chemically by reintroduction of the wild-type Hlcys3 gene in the mutant and by exogenously supplying methionine during mutant infection, respectively. These findings establish pathogen sulfur metabolism as a basic compatibility factor for this disease. The role of basic compatibility was further explored by establishing the temporal-spatial and morphological dynamics of tree host colonization by H. lauricola in comparison with the nonpathogenic species H. aguacate. The nonpathogen was able to colonize Lauraceae hosts at and adjacent to the inoculation zone, similarly to the pathogen, but was unable to systemically colonize trees. Differences in these colonization patterns were not associated with the timing or magnitude of tylosis development at the infection point. These findings indicate that basic compatibility for niche occupation must be coupled with specific compatibility factors for systemic colonization and symptom development. Determining the universality of these findings in other vascular tree wilting diseases may suggest strategies for mitigating tree mortality in ecosystems and agriculture. [Formula: see text] Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.