Molecular Plant-microbe Interactions最新文献

Zymoseptoria tritici causes Septoria tritici blotch, which significantly reduces yields of wheat. To investigate infection phase-specific gene expression in the pathogen, we analyzed gene expression during infection of susceptible and resistant wheat cultivars, as well as the nonhost species barley, at 1, 3, 6, 10, 17, and 23 days postinoculation (DPI). There were dramatic differences in pathogen gene expression at 10 DPI in the susceptible compared with both resistant interactions. The most pronounced differences in pathogen gene expression were observed at 3 DPI in both the susceptible and resistant host interactions compared with the nonhost. Thirty-one putative effectors showed early expression during the susceptible compared with the nonhost interaction; six were selected for subcellular localization studies. Using Agrobacterium-mediated transient expression in Nicotiana benthamiana, subcellular localization assays revealed that two candidate effectors localized to putative mobile cytosolic bodies when expressed without their signal peptides, suggesting potential roles in intracellular signaling or host gene regulation. When expressed with their signal peptides, four candidate effectors localized to the cytosol, whereas one did not accumulate to detectable levels. Comparison of pathogen gene expression in the susceptible host with expression in the resistant hosts identified genes expressed during the transition from biotrophic to necrotrophic growth at 10 DPI. Comparison of pathogen gene expression in resistant and susceptible hosts, versus in the nonhost barley, identified genes involved in initial colonization and host recognition. These results contribute to understanding candidate effectors that are activated early during infection and may play a role in the suppression of plant immunity. [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.

The composition of the plant microbiome is shaped not only by the host plant and abiotic environmental factors, but also by inter-microbial cooperation and competition. Plant pathogens, therefore must remain competitive within the microbiome in order to establish themselves within their host niche. Magnaporthe oryzae, the blast-disease causing ascomycete fungus, is able to 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-defence 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 over-representation of genes encoding drug efflux transporters, hydrolases, signalling components, DNA repair and oxidative stress responses. This indicates 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.

Fusarium wilt of strawberry, caused by the soilborne fungal pathogen Fusarium oxysporum f. sp. fragariae (Fof), is one of the greatest threats to cultivated strawberry. The pathogen penetrates strawberry plants through roots, severely affecting roots and crowns and resulting in rapid wilting and death. Research into the genetic basis of resistance to Fof has identified five loci, FW1 to FW5, that confer resistance to Fusarium wilt of strawberry and one Fof effector, SIX6. Although it is hypothesized that FW1 recognizes the SIX6 effector, the underlying resistance gene is unknown. A new isolate of Fof that breaks FW1-mediated resistance recently emerged and poses a significant threat to the California strawberry industry, the source of 88 to 91% of the strawberries produced in the United States. There are still significant gaps surrounding the molecular and physiological interaction between Fof and strawberry and the evolution of pathogenicity of Fof isolates unaffected by FW1. This review summarizes our current knowledge, identifies knowledge gaps, and provides a summary of genomic and molecular tools currently available to study the Fof-strawberry interaction. [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.

Plants recognize pathogen-associated molecular patterns via pattern recognition receptors, leading to the activation of pattern-triggered immunity in response to pathogen attack. Phytophthora infestans ceramide D (Pi-Cer D) is a sphingolipid from the oomycete pathogen P. infestans. Pi-Cer D is cleaved by the plant extracellular ceramidase NEUTRAL CERAMIDASE 2 (NCER2), and the resulting 9-methyl-branched sphingoid base is recognized by the plant receptor RESISTANT TO DFPM-INHIBITION OF ABSCISIC ACID SIGNALING 2 (RDA2) at the plasma membrane to transduce a defense signal. However, additional components are likely involved in sphingolipid recognition, which remain to be identified. Here, we employed a screen based on Lumi-Map technology to look for Arabidopsis (Arabidopsis thaliana) mutants with altered defense responses to Pi-Cer D. We identified three mutants showing diminished responses to Pi-Cer D and elf18, each carrying mutations in STAUROSPORIN AND TEMPERATURE SENSITIVE 3-LIKE A (STT3A), which encodes an oligosaccharyltransferase. The stt3a mutants exhibited higher susceptibility to the pathogen Colletotrichum higginsianum than the wild type. In stt3a mutants, the molecular mass of NCER2 and RDA2 proteins appeared smaller, indicating that STT3A is involved in posttranslational modification of the proteins. An enzymatic deglycosylation assay revealed that NCER2 and RDA2 are N-glycosylated. These findings suggest that STT3A contributes to plant immunity via posttranslational modification of proteins including NCER2 and RDA2. [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.

Plasmodiophora brassicae, the obligate parasite responsible for clubroot in Brassica crops and other crucifers, poses a major challenge to sustainable disease management due to its biotrophic lifestyle and adaptability. Recent advances in genomics, transcriptomics, and bioinformatics have accelerated the identification of its effector repertoire, which underpins host colonization and symptom development. To date, more than 100 putative effectors have been described, including several that modulate key plant defense processes such as pattern-triggered immunity, programmed cell death, phytohormone signaling, and ubiquitin-mediated protein degradation. Despite the inability to culture or genetically manipulate P. brassicae, functional studies using heterologous systems and transgenic approaches have revealed important insights into effector activity and host-pathogen interactions. Notably, conserved effectors such as PbBSMT and PbZF1 play central roles in virulence, highlighting their potential as targets for resistance breeding and effector-informed management strategies. However, the majority of candidate effectors remain uncharacterized, and inconsistent naming conventions across studies complicate cross-comparison. This review provides the first comprehensive synthesis of current knowledge on P. brassicae effectors, aiming to classify them according to their roles in host manipulation. Putative effectors that are consistently expressed across life cycle stages and host systems were identified and may serve as candidates for future investigation. We also discuss methodological advances and limitations in effector discovery and functional analysis, as well as opportunities to leverage effector biology in clubroot management. Ultimately, classifying conserved versus accessory effectors and understanding their interactions with host targets will be key to developing durable resistance and innovative strategies for clubroot management. [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.

Arbuscular mycorrhizal (AM) symbiosis is an ancient association that played a key role in the adaptation of plants to terrestrial environments. Originating over 400 million years ago at the dawn of land plants, this interaction depends on a core set of conserved genes that enables hosts to establish and maintain symbiotic relationships with AM fungi. The AM symbiotic program includes distinct genetic components for each stage of development, from signal perception to nutrient exchange. Whereas AM host plants have retained key genes dedicated to symbiosis, nonhost lineages have independently lost these genes multiple times over evolutionary history. Recent studies on the liverwort Marchantia paleacea demonstrate that core mechanisms underlying AM symbiosis are conserved from bryophytes to angiosperms. Comparative genomic studies continue to uncover how symbiosis-specific genes are integrated with broadly conserved cellular machinery to sustain this interaction. Understanding these deeply conserved genetic modules is essential for uncovering the evolutionary foundations of plant-microbe associations and for harnessing their potential in sustainable agriculture. [Formula: see text] Copyright © 2025 The Author(s). This is an open access article distributed under the CC BY 4.0 International license.

CRISPR-Cas genome editing is a powerful tool for understanding the pathogenicity of oomycetes, a group that includes several destructive plant parasites. Although a few Phytophthora species have benefited from plasmid-based transformation methods for gene overexpression and RNA interference silencing, these techniques remain inefficient for other oomycete genera such as Pythium and Aphanomyces. Here, we explored the applicability of DNA-free endogenous counterselection in filamentous oomycetes, using CRISPR-Cas9 ribonucleoproteins (RNPs). We used biolistics to deliver RNPs targeting the adenine phosphoribosyltransferase (APT) gene and generated selectable 2-fluoroadenine-resistant mutants in Aphanomyces, Pythium, and Phytophthora species. Targeted mutagenesis resulted in various deletions at the expected cut sites, confirming efficient genome editing. Knockout mutants exhibited no alterations in growth or virulence, making APT a suitable selectable marker gene for oomycete research. Whole-genome comparative analyses on CRISPR-edited mutants revealed no or very few additional mutations in A. euteiches and Pythium oligandrum and substantial off-target effects in Phytophthora capsici. This one-step approach circumvents the need for protoplast generation and can be broadly applied to oomycetes producing zoospores or oospores. [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.

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.

Invasive, lethal tree diseases continue to have devastating effects on forest ecology, commercial timber production, horticulture 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 up-regulation 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 non-pathogenic species H. aguacate. The non-pathogen was able to colonize Lauraceae hosts at and adjacent to the inoculation zone similar to the pathogen but was unable to systemically colonize trees. Differences in these colonization patterns were not associated with the timing or magnitude of tyloses 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.

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.