Molecular Plant-microbe Interactions最新文献

Heterosis is the increased performance of hybrids relative to their parental genotypes. Heterosis for growth may be mediated by underlying traits, including traits affecting host-microbe interactions. A trade-off between growth and defense is often observed in plant disease studies, such that a stronger defense response is often associated with slower growth and lower yield. We investigated the production of reactive oxygen species (ROS) following treatment with microbial elicitors, an early component of the pattern-triggered immunity (PTI) response, in maize hybrids and their inbred parents. ROS production was often reduced in hybrids compared to inbred parents, and this effect was dependent on genotype, elicitor used, and time of day. These results identify PTI as a response displaying heterosis whose regulation might contribute to heterosis in other traits such as growth and yield.

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.

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.

The soybean cyst nematode (SCN), Heterodera glycines, remains the most damaging pathogen of soybean worldwide. Genomic advances over the past two decades have transformed our understanding of both the nematode and its host. On the soybean side, genome sequencing, pangenome development, and multi-omics studies have clarified how classical resistance loci such as Rhg1 and Rhg4 function while also revealing a broader and more complex landscape of resistance mechanisms. On the nematode side, effector discovery, high-quality genome assemblies, and evolutionary analyses have shed light on how SCN adapts to resistant cultivars and remodels host cellular processes. Despite these advances, overreliance on a single resistance source, PI 88788, continues to accelerate virulence shifts in SCN populations. This underscores the urgent need for diversified resistance, improved monitoring of nematode adaptation, and deeper mechanistic insight into the interaction. In this review, we integrate current knowledge of soybean-SCN interactions across genomics, transcriptomics, proteomics, cell biology, and microbiome research. We highlight how integrative functional genomics is reshaping the discovery of resistance genes, clarifying nematode virulence strategies, and guiding the development of more durable management approaches. Finally, we outline emerging directions, including pangenomics, dual host-pathogen analyses, and predictive breeding, that are expected to advance innovation in SCN control. [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.

Harnessing root-associated microbiomes to promote beneficial microbial compositions could offer a sustainable strategy to increase crop resilience. Major challenges impeding this strategy are the lack of understanding of which native members of the microbiome benefit the host and the molecular signaling events underlying these benefits. In this study, we isolated a strain of Roseateles chitinivorans, RcP500, corresponding to the most abundant bacterial taxon in the switchgrass root microbiome. Inoculation of roots with RcP500 promoted growth and induced systemic resistance (ISR) to Bipolaris leaf spot of switchgrass and closely related Panicum hallii. R. chitinivorans is also highly abundant in the rhizosphere and root microbiomes of maize and rice and enhanced the growth of these two plant species. Furthermore, RcP500 elicited ISR in maize against anthracnose leaf blight and southern corn leaf blight. Bioassays and root metabolite profiling in maize wild-type and jasmonic acid (JA)-deficient opr7opr8 mutant plants revealed the requirement of JA-dependent processes in RcP500-elicited synthesis of the JA precursor, 12-OPDA (cis-(+)-12-oxo-phytodienoic acid), and an α-ketol, 9,10-KODA (9-hydroxy-10-oxo-12(Z)-octadecadienoic acid), two oxylipins previously implicated in ISR signaling. Xylem sap transfusion of RcP500-colonized plants to naïve receiver plants corroborated the role of JA in promoting these signaling intermediates. Whereas root JA synthesis was downregulated upon RcP500 colonization, gibberellic acid was induced, suggesting a potential mechanism behind the simultaneous growth promotion and ISR triggered by this bacterium. Overall, this study identified a novel rhizobacterium with a broad host range that promotes growth and systemic resistance across multiple plant species in a JA-dependent, ketol-driven manner. [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.

The nitrogen-fixing symbiosis between leguminous plants and soil bacteria, collectively termed rhizobia, is a major contributor of fixed nitrogen to the biosphere. The ability of legumes to secure nitrogen from the atmosphere underlies their ecological success and has made them important crops in both traditional and modern sustainable agriculture. Many genes directing the establishment and functioning of this beneficial interaction have been identified under laboratory conditions using a limited number of bacterial strains and plant species in pairwise combinations. Under natural and field conditions, however, plants encounter numerous potential partners, as soil microbiomes contain diverse bacteria equipped with the necessary toolkit for symbiosis. Consequently, legumes must possess mechanisms to select for or against specific partners. This review highlights how legumes employ elements of their immune system for the negative selection of rhizobia via processes resembling the gene-for-gene model of effector-triggered immunity in plant-pathogen interactions. [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.

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.

The necrotrophic fungal pathogen Sclerotinia sclerotiorum is distinguished by its exceptionally broad host range, infecting numerous plant species across diverse genera. Although historically characterized by a seemingly unspecialized infection strategy, increasing evidence indicates that S. sclerotiorum employs a diverse suite of virulence mechanisms, including effectors for host and environment manipulation. Leveraging recent advances in structural genomics and the growing availability of genomic and transcriptomic resources, we systematically re-examined the effector repertoire of the reference strain 1980 using updated computational approaches. We identified 215 effector-like proteins, which were classified into structural families based on predicted tertiary structures. Transcriptome meta-analysis across hundreds of publicly available samples revealed diverse expression patterns among effectors, highlighting both conserved and condition-specific expression dynamics. Several effector families were found to be expanded in S. sclerotiorum, including groups with predicted antimicrobial functions and unique domain architectures. Within families, structural and surface property variation suggests potential functional diversification. Furthermore, coexpression network analysis uncovered putative gene clusters that may operate synergistically with selected effectors. This work refines our understanding of effector diversity and organization in S. sclerotiorum and provides a framework for prioritizing candidates for functional studies, ultimately contributing to the broader understanding of effector evolution in generalist fungal pathogens. [Formula: see text] Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY 4.0 International license.

The composition of the plant microbiome is shaped not only by the host plant and abiotic environmental factors, but also by intermicrobial cooperation and competition. Plant pathogens, therefore, must remain competitive within the microbiome to establish themselves within their host niche. Magnaporthe oryzae, the blast disease-causing ascomycete fungus, can infect economically important hosts including rice, barley, and wheat. We sought to identify barley-associated bacteria able to antagonize M. oryzae and to characterize the fungal transcriptional responses following confrontation to reveal antimicrobial self-defense mechanisms. From a library of 25 barley-associated bacteria, two strains were identified as moderate and strong antagonists. Through RNA-seq, we demonstrate large-scale transcriptional changes in M. oryzae during their confrontation. Common responses to both strains included an overrepresentation of genes encoding drug efflux transporters, hydrolases, signaling components, DNA repair, and oxidative stress responses. This indicates that M. oryzae prioritizes stress adaptation and detoxification. We did not observe a significant increase in secreted proteins of M. oryzae as part of the common response. However, significant strain-specific changes were observed, indicating that, independent of host plant, specific microbial antagonists are perceived by M. oryzae, leading to altered secretome profiles. Understanding these adaptive strategies provides insight into antimicrobial resistance mechanisms with respective parallels to drug- and fungicide-resistance mechanisms in the medical and agricultural context. Additionally, our study provides potential targets on the plant pathogen side to weaken its fitness within the plant microbiome. [Formula: see text] Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY 4.0 International license.

Plant resistance (R) and pathogen avirulence (Avr) gene interactions are central to pathogen recognition and disease resistance in crops. Functional characterisation of recognised 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 defence responses in a set of diverse wheat cultivars. We identified an Avr candidate, termed AvrPstB48, that triggers defence 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 defences and enabled us to identify a single amino acid in AvrPstB48 that is necessary but not sufficient for defence activation. Notably, the activation of defence signalling by AvrPstB48 in protoplasts did not directly correlate with disease outcomes. Whole-plant infection assays revealed that some cultivars which exhibited strong defence activation in the protoplast assay are susceptible to the Pst isolate Pst104E137A- from which AvrPstB48 is derived. Comparison of infection dynamics of two wheat cultivars that differ in their AvrPstB48 recognition capacity revealed a delay in disease progression in the recognising cultivar Avocet S compared to the non-recognising cultivar Morocco. While correlative only, our observations, combined with other recent reports, support a 'recognize-then-suppress' model of plant-pathogen interaction where disease outcomes are driven not only by simple Avr/R interactions but also by pathogen effectors that suppress defence signalling downstream of effector recognition.