Molecular Plant-microbe Interactions最新文献

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.

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.

Reactive oxygen species (ROS) play a central role in plant defense, especially during interactions with plant-parasitic nematodes (PPNs). These molecules act as early signals that activate immune responses and help reinforce plant cell walls to block nematode invasion. However, PPNs have evolved specialized effector proteins (small, secreted molecules, typically proteins, that enter host cells to directly suppress immunity and manipulate host processes), which they secrete into host tissues and cells to interfere with ROS production and signaling. These effectors can suppress ROS bursts, detoxify reactive molecules, or manipulate host pathways to reduce immune responses. This review synthesizes current knowledge on these effector-driven strategies, from their discovery using advanced genomics to their specific molecular mechanism of ROS suppression. We also explore the critical interplay between ROS signaling and plant hormone pathways during infection, and provide an overview of the key techniques used to detect and quantify ROS in plant-nematode interactions.

Potato mop-top virus (PMTV) is a significant pathogen causing potato "spraing" disease worldwide. The PMTV 8K protein functions as a weak viral suppressor of RNA silencing (VSR), has viroporin activity and plays a role in pathogenicity by promoting viral long-distance movement and modulating host responses. Uniquely, PMTV can establish systemic infection in the absence of the 8K protein, though the infection is slightly delayed. To elucidate the molecular mechanisms underlying PMTV-host interactions, we conducted comprehensive RNA-seq analysis comparing wild-type PMTV with a mutant lacking the 8K gene (PMTV-Δ8K) in Nicotiana benthamiana. Our transcriptomic analysis shows that wild-type PMTV and PMTV-Δ8K elicit largely distinct transcriptional responses in the host, with more unique than shared differentially expressed genes. The analysis also revealed extensive reprogramming of metabolic pathways, stress responses, and defense mechanisms. Notably, wild-type PMTV induced more defense-related transcription factors, including 27 WRKY genes compared to 8 in PMTV-Δ8K infections. RNA silencing pathway genes displayed distinct expression patterns, with AGO2, RDR1, and AGO-MEL1 showing notably enhanced upregulation (up to 9.7-fold) in PMTV-Δ8K infections. Functional analysis identified chloroplast-associated genes GNS2, CHUP1, and KIN5l as host restriction factors. Virus-induced gene silencing experiments confirmed that GNS2 and CHUP1 restrict viral accumulation under both infection scenarios (wild-type PMTV and PMTV-Δ8K), while localization studies revealed that TGB2 protein and GNS2 co-localize at chloroplast structures. These findings provide insights into PMTV pathogenesis, suggest that 8K is a multifunctional protein operating through diverse mechanisms, and advance understanding of viral suppression strategies.

Sugarbeet provides an important source of sucrose; a stable, environmentally safe, and low-cost staple in the human diet. Viral diseases arising in sugarbeet ultimately impact sugar content, which translates to financial losses for growers. To manage diseases and prevent such losses from occurring, it is essential to characterize viruses responsible for disease. Recently, our laboratory identified a tobacco necrosis virus A variant named Beta vulgaris alphanecrovirus 1 (BvANV-1) in sugarbeet roots. We validated the infectivity of BvANV-1 using two DNA-based clones; one sequence referred to as wild type and another as mutant #7 that harbors one non-synonymous and one synonymous mutation in the viral replicase gene (p23) and one synonymous mutation in the p8 movement protein gene relative to wild type. The host range of the virus was determined through inoculating a series of local weed species and agriculturally relevant hosts, which showed that soybean and pinto bean are potentially important hosts of this virus. Using both clones, viral transmission to sugarbeet by Olpidium virulentus was verified. Using site-directed mutagenesis of mutant #7, we demonstrated that the amino acid change in the p23 gene alone restored the phenotype similar to wild type on Nicotiana benthamiana inoculated leaves. Additionally, this latter change and the synonymous mutation in the p8 gene were both required to re-establish systemic infection in N. benthamiana similar to wild type. Our analysis reveals differences among both variants and lays the groundwork for characterizing the role of BvANV-1 proteins during infection.

In a previous DNA-based microbiome study of grapevines in areas of Pierce's disease (PD) pressure, we determined that taxa belonging to the Pseudomonas and Achromobacter genera negatively associated with PD severity and titer of the causal agent, Xylella fastidiosa, leading us to hypothesize that these taxa suppress PD and could be deployed as biocontrols. Here, we tested this hypothesis using two bacterial isolates from the grapevine endosphere, Pseudomonas viridiflava and Achromobacter vitis. We demonstrate that pretreatment with these two isolates significantly reduced PD symptoms and X. fastidiosa titer, comparable to that of a known PD biocontrol agent, Paraburkholderia phytofirmans PsJN. We monitored early spatial transcriptional responses using genome-wide transcriptional profiling in vines that were pretreated with the biocontrol strains and then inoculated with X. fastidiosa. We coupled this with phenotyping of internal tylose development and external disease symptoms and bacterial titer and determined that grapevines pretreated with the biocontrols A. vitis and PsJN developed fewer tyloses and PD symptoms and underwent major transcriptional reprogramming in response to X. fastidiosa. These included upregulation of genes in auxin- and ethylene-signaling pathways linked to tylose development. In contrast, P. viridiflava pretreatment also resulted in a reduction of tyloses and PD symptoms but did not induce major transcriptional changes in vines, suggesting that it likely has a direct inhibitory effect on X. fastidiosa through antibiosis. Using these data, we propose a model that incorporates timely and effective deployment of tyloses driven by induction of ethylene and auxin pathways as a key factor in PD resistance. [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 recent discovery of the lanthanide(Ln)-dependent methanol dehydrogenase (Ln-MDH) XoxF has expanded the spectrum of bacteria recognized for methylotrophic metabolism. Many bacteria, including rhizobia, have historically escaped being categorized as methylotrophs because they exclusively produce XoxF-type Ln MDHs and entirely lack the long-studied calcium-dependent methanol dehydrogenase MxaFI. We report that the XoxF-type Ln-MDH encoded by the smb20173 gene is the sole methanol dehydrogenase that supports methylotrophic growth of Sinorhizobium meliloti. The lanthanides that consistently supported growth of S. meliloti in minimal media with methanol included lanthanum, cerium, praseodymium, and neodymium. Based on genome, whole-transcriptome, and mutant phenotype analyses, we propose a metabolic model for Ln-dependent methylotrophy in S. meliloti wherein oxidation of one-carbon compounds, such as methanol, generate the reducing power needed to assimilate carbon via the Calvin-Benson-Bassham cycle. By investigating how these newfound insights about lanthanides reshape our understanding of the methylotrophic capabilities of rhizobia, we explored how methanol produced by plants has the potential to create a nutritional niche in the rhizosphere. Using a Medicago sativa (alfalfa) nodule occupancy assay, we found that a xoxF mutant strain was outcompeted by the wild-type strain only when lanthanides were available, suggesting that Ln-dependent methylotrophy promotes an efficient rhizobia-legume symbiosis.

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.