Molecular Plant-microbe Interactions最新文献

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.

We applied dual-organism single-nucleus transcriptomics to study the interaction between grapevine leaves and Erysiphe necator, the causal agent of powdery mildew, at 1 and 5 days postinfection, including controls and three biological replicates. We generated a grapevine leaf atlas encompassing over 100,000 nuclei and a pathogen atlas of more than 3,000 nuclei. We successfully annotated all major grapevine cell types, including mesophyll, epidermis, phloem and xylem parenchyma, companion cells, and guard cells. We identified key E. necator structures, including appressoria, haustoria, and hyphae and provided a list of novel cell type markers for both species. We reveal structure-specific gene expression programs in E. necator, laying a foundation for future studies of fungal development and virulence mechanisms. In the host, we identified spatially distinct expression patterns of defense-related genes. As the infection progressed, we observed the activation of a coordinated immune response involving multiple cell types, mainly epidermal and mesophyll cells. High-dimensional weighted gene co-expression network analysis identified key hubs and networks associated with cell type-specific signaling and defense response. We describe a spatial separation of pattern- and effector-triggered immunity, supporting a model in which pattern-triggered immunity is activated at the site of pathogen contact and effector-triggered immunity is induced in surrounding tissue. [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.

To successfully colonize the living tissue of its host, the fungal wheat powdery mildew pathogen produces diverse effector proteins that are suggested to reprogram host defense responses and physiology. When recognized by host immune receptors, these proteins become avirulence (AVR) effectors. Several sequence-diverse AVRPM3 effectors and the suppressor of AVRPM3-PM3 recognition (SVRPM3^a1/f1) are involved in triggering allele-specific, Pm3-mediated resistance, but the molecular mechanisms controlling their function in the host cell remain unknown. Here, we describe that AVRPM3^b2/c2, AVRPM3^a2/f2, and SVRPM3^a1/f1 form homo- and heteromeric complexes with each other, suggesting that they are present as dimers or higher-order multimers in the host cell. Alphafold2 modeling substantiated previous predictions that AVRPM3^b2/c2, AVRPM3^a2/f2, and SVRPM3^a1/f1 all adopt a core RNase-like fold. We found that a single amino acid mutation in a predicted surface-exposed region of AVRPM3^a2/f2 resulted in recognition by the PM3b immune receptor, which does not recognize wild-type AVRPM3^a2/f2. This indicates that differential AVRPM3 recognition by variants of the highly related PM3 immune receptors is due to subtle differences in similar protein surfaces of sequence-diverse AVRs. Our study reveals complex molecular interactions between powdery mildew effectors. These findings suggest that structural similarity, rather than sequence conservation, underlies both the promiscuous multimerization of these effectors and their recognition by specific PM3 immune receptors. [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.

When disease resistance was still viewed as a vague physiological response rather than a genetically defined process, Harold Henry Flor laid the foundation for our modern understanding of plant immunity with his gene-for-gene concept. Initially developed for simple host-pathogen interactions, this idea has evolved into a more complex framework in which plants engage in continuous dialogue with a diverse microbiome. Within this community, beneficial, commensal, and pathogenic microbes interact both directly and indirectly through the plant host, extending the boundaries of plant immunity beyond the individual organism. This broader perspective envisions an "extended plant immune system" that integrates the plant's microbial partners into a coordinated, community-level defense. Like early views of disease resistance, this concept was first described in broad physiological or ecological terms. As the field has matured with the advent of next-generation sequencing, it has become clear that the microbiome-mediated extension of the plant immune system is also grounded in genetically determined molecular processes. These range from host-driven recruitment of protective microbiota to microbial traits that suppress pathogens, and to plant mechanisms that enable beneficial microbes to trigger induced systemic resistance. This review is a symphony composed of the historical progression of research from molecular recognition to community-level defense, distilling the principles that connect classical plant immunity with emerging plant-microbiome concepts and framing microbiome-mediated disease protection as an extension of the plant's innate immune system. This integrated perspective not only reframes our understanding of plant immunity but also offers a conceptual foundation for harnessing the extended immune system in sustainable crop protection. [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.

Rice blast is caused by the fungus Magnaporthe oryzae and seriously threatens rice production worldwide. Harnessing microbe-mediated resistance is a key strategy in disease control. The RBL1 gene of rice encodes a cytidine diphosphate diacylglycerol synthase, and editing of RBL1 resulted in a new allele named RBL1^Δ12, which confers multipathogen resistance and maintains yield. This study demonstrated that enhanced blast resistance of rbl1^Δ12 partially stemmed from differences in phyllosphere microbiota. The rbl1^Δ12 line exhibited enrichment of beneficial microorganisms in the phyllosphere, such as those from the genera Pantoea, Pseudomonas, Acidobacteria, and Sphingomonas, which inhibited the growth of several rice pathogens in dual culture plates. Moreover, phyllosphere microbial interactions were strengthened in rbl1^Δ12, contributing toward resistance to M. oryzae. Synthetic microbial communities that mimic rbl1^Δ12 microbial communities induced rice immunity and enhanced the resistance to M. oryzae in two rice varieties, achieving environmentally friendly control of rice blast. This study revealed that host genetic modification contributed to shaping microbiome composition, providing a strategy based on beneficial microbes for sustainable disease control. [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 lipid transfer proteins (LTPs), belonging to the pathogenesis-related protein 14 family, participate in plant immune response to biotic stress. LTP1 from Vigna unguiculata was previously shown to be able to suppress infection by cowpea mosaic virus and soybean mosaic virus. However, whether cowpea LTP1 participates in the plant resistance to other plant pathogens remains unclear. The present study analyzed the role of LTP1 in plant resistance to eukaryotic pathogens. We observed that LTP1 overexpression in cowpea and tobacco significantly reduced the lesion areas and biomass of the fungus Botrytis cinerea and oomycete Phytophthora capsici. A protein lipid overlay assay showed that LTP1 bound phosphatidic acid and phosphatidylinositol (4,5)-bisphosphate, but LTP1^3A, with three amino acids in the lipid-binding domain being mutated to alanine, lost its lipid-binding ability. Consistently, overexpression of LTP1^3A did not influence lesion area and pathogen biomass in cowpea and tobacco plants after inoculation with B. cinerea at 48 h postinoculation. LTP1 heterologous expression in tobacco induced a significant increase in intracellular calcium, inositol 1,4,5-trisphosphate (IP₃) levels, and abscisic acid contents, leading to more significant stomatal closure after B. cinerea infection. Overall, our findings suggest that cowpea LTP1 participates in the plant defense response through interacting with specific phospholipids, thereby interfering with pathological processes such as IP₃-mediated calcium signaling and stomatal movement. [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.

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.

Three major components of lipopolysaccharide in rhizobia, namely core polysaccharide, o-antigen, and lipid A, often act as microbe-associated molecular patterns to participate in the symbiosis between rhizobia and legumes. Rhizobia have a different lipid A structure from other gram-negative bacteria. The 3-hydroxy group on the 2' or 3' myristate acyl chain of its lipid A is substituted by a unique very-long-chain fatty acid (VLCFA), 27-hydroxyoctacosanoic acid. VLCFAs are usually transferred to lipid A by an acyltransferase, MsbB. In this research, we constructed an msbB deletion mutant and complementary and overexpression strains of Sinorhizobium fredii HH103 and investigated their free-living and symbiotic phenotypes. The findings revealed that deletion of msbB had no impact on the autonomous growth of HH103 yet significantly reduced the resistance of rhizobia to abiotic stresses. Promoter-GUS assays revealed that msbB was mainly expressed at the early stage of nodulation. Quantitative analysis of early infection events revealed that the mutation of msbB significantly reduced root hair curling, infection threads, and nodule primordia, suggesting impairment of the symbiotic infection process. Nodulation assay and transmission electron microscopy analysis of the nodule ultrastructure further showed that msbB deletion led to the formation of small and ineffective root nodules without colonization of rhizobia, thereby causing a loss of nitrogen fixation capacity. RNA-seq analysis indicated that HH103ΩmsbB inoculation may impair early symbiotic signaling and trigger a localized defense response in the soybean root to result in symbiotic deficiencies. Taken together, these results reveal the important role of VLCFAs in soybean rhizobia in the establishment of effective symbiosis and nodule nitrogen fixation. [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 establish beneficial associations with microbiota, enhancing their resilience to environmental challenges. FERONIA (FER) kinase shapes the microbiome; despite extensive knowledge of FER interactors that regulate development and immunity against pathogens, the specific partners involved in microbiome modulation remain underexplored. Through a reverse genetic screen of Arabidopsis leucine-rich repeat extensin (LRX) genes, which encode FER-interacting cell wall sensors, we found that loss of function of lrx1/2 leads to enriched rhizosphere Pseudomonas, similar to fer mutants. 16S rRNA sequencing revealed that, when grown in natural soil, lrx1/2 and fer-4 have similarly altered rhizosphere microbiomes with decreased bacterial diversity. Notably, lrx1/2 and fer-4 mutants both exhibit growth defects in high pH natural soil that could be rescued by lowering the soil pH and increasing phosphate. Microbiome sequencing under conditions that rescued fer-4 and lrx1/2 stunting showed that the altered microbiome of lrx1/2 and fer-4 persists independently of changes in plant growth. This indicates that FER and LRX1/2 play an integral role in shaping the rhizosphere microbiome. [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.

Molecular interactions between aphids and plants include delivery of salivary effector proteins into host cells, acting as virulence factors to suppress host immunity, or as avirulence functions triggering immune activation. However, understanding of virulence and avirulence mechanisms in aphid-plant systems is currently limited. Here, we report discovery of an effector candidate family that is unique to aphids. Using functional genomics data on divergent pea aphid (Acyrthosiphon pisum) genotypes and their F1 progeny, we filtered for differentially expressed saliva proteins that co-segregated with virulence or avirulence phenotypes. LOC100575698 (ACPISUM_029930), annotated as an uncharacterized protein, was the sole candidate effector for which RNA-Seq and saliva proteomics data showed significantly different expression both between avirulent and virulent parents and between their segregating F1 progeny, with this gene upregulated in avirulent genotypes. BLASTP searches revealed multiple divergent homologs only in genomes of the Aphidomorpha infra-order, suggesting a hitherto undefined ancient aphid-specific gene family. AlphaFold models indicate strong structural similarities but weak sequence homology to chitinases. Because the aphid-specific clade all lack canonical DxxDxDxE motifs for catalytic activity, we designate the proteins as a novel CHitinase-Like (CHL) family. Association of ACPISUM_029930 (ApCHL1) with avirulence was further supported by co-segregating SNPs and a genotype-specific alternatively spliced isoform. We hypothesise that CHL proteins may function similarly to phylogenetically unrelated chitin-binding fungal effectors that sequester chitin, also present in aphid stylets, potentially preventing defence activation through plant chitin receptors and/or blocking chitin degradation by host-secreted chitinases.