Molecular Plant-microbe Interactions最新文献

The necrotrophic pathogen Alternaria alternata produces a host-selective toxin to attack its host plants. This study characterized the crucial function of the Mip1/RAPTOR ortholog (AaMip1) in toxin production and autophagy formation. AaMip1 physically interacts with the Target of Rapamycin (Tor) protein. In response to nitrogen starvation and hydrogen peroxide (H₂O₂), AaMip1 binds to Tor and triggers autophagy and oxidative stress detoxification. Deleting the AaMip1 gene resulted in a ΔAaMip1 strain that increased sensitivity to various oxidants; decreased the expression of two oxidative-stress-response genes, AaYap1 and AaNoxA; and had lower catalase activity than the wild type. ΔAaMip1 produced lower levels of ACT toxin than the wild type after a 7-day incubation; however, ΔAaMip1 produced tricycloalternarene mycotoxins but not ACT after 21 days. The reduction of ΔAaMip1 virulence in the host plant is due to low ACT production, defective H₂O₂ detoxification, impaired autophagy, and slow growth during invasion. However, AaMip1 plays a negative role in maintaining cell wall integrity and lipid body accumulation. ΔAaMip1 had thicker cell walls and emitted brighter red fluorescence after staining with the cell-wall-disrupting agents Congo red and calcofluor white. ΔAaMip1 was more resistant to these compounds than the wild type under nutrient-rich conditions. The observed defects in the ΔAaMip1 were restored in the complementation strain after re-expressing a functional copy of AaMip1. This study increases our understanding of how A. alternata deals with toxic reactive oxygen species, triggers autophagy formation, maintains normal cell wall integrity, and regulates toxin metabolism via the AaMip1-mediated signaling pathways. [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.

Xanthomonas oryzae pv. oryzae (Xoo), the causal agent of bacterial blight of rice, translocates multiple transcription activator-like effectors (TALEs) into rice cells. The TALEs localize to the host cell nucleus, where they bind to the DNA in a sequence-specific manner and enhance gene expression to promote disease susceptibility. Xoo strain PXO99^A encodes 19 TALEs, but the host targets of all these TALEs have not been defined. A meta-analysis of rice transcriptome profiles revealed a gene annotated as flavonol synthase/flavanone-3 hydroxylase (henceforth OsS5H/FNS-03g) to be highly induced upon Xoo infection. Further analyses revealed that this gene is induced by PXO99^A using Tal9b, a broadly conserved TALE of Xoo. Disruption of tal9b rendered PXO99^A less virulent. OsS5H/FNS-03g functionally complemented its Arabidopsis homologue AtDMR6, a well-studied disease susceptibility locus. Biochemical analyses suggested that OsS5H/FNS-03g is a bifunctional protein with salicylic acid 5' hydroxylase (S5H) and flavone synthase-I (FNS-I) activities. Further, an exogenous application of apigenin, the flavone that is enzymatically produced by OsS5H/FNS-03g, on rice leaves promoted virulence of PXO99^A tal9b^-. Overall, our study suggests that OsS5H/FNS-03g is a bifunctional enzyme, and its product, apigenin, is potentially involved in promoting Xoo virulence. [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 interaction between Sinorhizobium meliloti and alfalfa is a well-studied model system for symbiotic establishment between rhizobia and legume plants. Proper utilization of carbon sources has been linked with effective symbiotic establishment in S. meliloti strain Rm1021. Previous work has shown that mutation of the gene tktA, which encodes a transketolase involved in the pentose phosphate pathway, resulted in a strain impaired in many biological functions, including the ability to establish symbiosis with alfalfa. Work with this strain revealed the appearance of suppressor mutations that could partially revert the symbiotic phenotype associated with a tktA mutation. Characterization of these suppressor strains showed that carbon phenotypes associated with a mutation in tktA were no longer present and that the production of succinoglycan was partially restored. Central carbon metabolite pools were observed to be different compared with the wild-type and tktA mutant strains. Multiple independent mutations were identified in the gene SMc02340, a Gnt-type negative regulator, upon sequencing. RT-PCR suggested that SMc02340 acts as a negative regulator on an operon containing the gene tktB, which becomes upregulated when the suppressor mutation is present or SMc02340 is removed. Microscopic analysis revealed a unique symbiotic phenotype. The tktA mutant strain induced root hair curling but could not colonize the apoplastic space. Collectively, the data suggest that the upregulation of tktB can partially bypass some blocks associated with a lesion in tktA, including the colonization of the curled root hair, but cannot fully compensate for the loss of tktA. [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.

Beet mosaic virus (BtMV) is one of several viruses infecting sugar beets and was previously managed by controlling the vector Myzus persicae with neonicotinoid seed treatment. Following the ban of this measure in 2019 in Europe, alternative control strategies needed to be researched. One alternative might be the use of RNA interference as a major antiviral defense system. Here, we report the selection of target regions using small RNA high-throughput sequencing of BtMV-infected Beta vulgaris subsp. vulgaris and Nicotiana benthamiana plants, the production of double-stranded RNA (dsRNA), and the effective use of dsRNA in inducing resistance against the mechanically inoculated virus under greenhouse conditions. In Escherichia coli HT115, the dsRNAs produced for BtMV P1 and nuclear inclusion body b (NIb) induced a high level of resistance when sprayed before mechanical BtMV inoculation, resulting in an 80% reduction of symptomatic B. vulgaris and N. benthamiana plants. Stem-loop RT-qPCR showed the systemic distribution of dsRNA-derived small interfering RNA molecules, but the applied dsRNA remained at the site of application and did not spread within the plant. However, when the virus was inoculated on the next upward leaf to the dsRNA application site, no protective effect was observed. Despite this limitation, the results demonstrate the potential of dsRNA as an effective tool for viral protection in sugar beets, thereby establishing a basis for future developments in systemic delivery and broader field applications. [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 Citrus sinensis LATERAL ORGAN BOUNDERIES 1 (CsLOB1) gene, which is directly induced by the Xanthomonas citri subsp. citri effector PthA4, functions as a transcription factor and citrus canker susceptibility (S) gene. Genome editing of CsLOB1 has been shown to confer resistance to citrus canker disease. Previous studies revealed that the citrus CsLOB1-INDUCED EXPANSIN 1 gene (CsLIEXP1) is highly and directly upregulated by CsLOB1 in Xanthomonas citri subsp. citri-infected plants. Because expansins are associated with cell wall loosening, potentially facilitating bacterial colonization, the CsLOB1-dependent activation of CsLIEXP1 is thought to contribute to canker symptoms and disease progression. Thus, CsLIEXP1 likely represents a critical canker susceptibility gene. In this study, we employed CRISPR/Cas9 to disrupt the function of CsLIEXP1 by modifying its corresponding coding region in Citrus sinensis cultivar 'Hamlin' and evaluated the postinfection responses of edited plants. DNA sequencing confirmed the edition of the CsLIEXP1-edited plant, which exhibited 26.47% of CsLIEXP1 edited sequences. Furthermore, CsLIEXP1 protein accumulation was reduced in CsLIEXP1-edited plants compared with the wild type when infected with X. citri. Leaves of edited plants inoculated with X. citri showed significantly fewer canker symptoms, with lesions limited to the site of bacterial inoculation and less pronounced cellular hypertrophy compared with control plants. Our results show that CsLIEXP1 is a citrus canker S gene that acts downstream of CsLOB1, thus providing new insights into plant-pathogen interactions. [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.

Quantitative disease resistance (QDR) is the most common form of disease resistance in crops, but it is challenging to understand at the cellular level due to the involvement of many genes and biological processes. Ralstonia solanacearum, the causal agent of bacterial wilt disease, is a destructive plant pathogen of Solanaceous species that is best controlled by quantitatively resistant varieties, but few QDR genes are known. We previously found that a tomato auxin pathway mutant known as diageotropica (dgt) has enhanced resistance to R. solanacearum. Here, we show that, as with wild-type quantitatively resistant tomato plants, resistance in dgt is the result of multiple mechanisms. Mock-inoculated dgt roots have endogenously higher levels of the plant defense hormone salicylic acid (SA). However, the SA-deficient double mutant dgtNahG is still resistant to R. solanacearum, indicating that SA-independent pathways are also required for resistance. Scanning electron microscopy revealed that R. solanacearum colonization of the root xylem is delayed in dgt. We found an increased number of lignified xylem cells and altered root vasculature anatomy in dgt, and dgt root length was not impacted by R. solanacearum treatment. Similar to the wilt-resistant wild-type tomato Hawaii7996, RNA sequencing results suggested that dgt may tolerate R. solanacearum-induced water stress better than the wilt-susceptible parent. Thus, resistance in dgt is due to several pathways, including preactivated SA defenses, physical barriers in the xylem, and an ability to tolerate water stress. The pleiotropic nature of this single mutation appears to mimic quantitative resistance. [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.

Verticillium longisporum, a soilborne fungal species, is the causative agent of Verticillium stripe disease in Brassica species and represents a notable threat to agricultural production, particularly in regions where oilseed rape is a major crop, including Europe, North America, and Asia. The microsclerotia of this pathogen can persist in the soil for extended periods, with a potential lifespan of up to a decade, thereby posing a substantial challenge for the complete eradication of the pathogen from infested soil. The genome of V. longisporum is amphidiploid and resulted from the hybridization of V. dahliae (D genotypes) and an unidentified species (A1 genotype). At least three independent hybridization events are estimated to have occurred, resulting in three distinct lineages: A1/D1, A1/D2, and A1/D3. Genome sequence analysis revealed the presence of mating-type idiomorphs, putative cell wall-degrading enzymes, and effectors. However, due to the complexity of the genome, there is a paucity of research on the molecular interactions between V. longisporum and Brassica crops. This review summarizes the extant knowledge regarding the pathogenicity factors that V. longisporum deploys upon infection and the host immune responses against this attack, highlighting aspects that remain to be elucidated and the molecular tools available for studying this interaction. A better understanding of the molecular interactions in this pathosystem will contribute to developing more effective control measures against this disease in Brassica oilseed and cabbage crops. [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.

Agrobacterium-mediated transient expression (AMTE) is an important tool in plant genetics studies and biotechnology. AMTE remains problematic in citrus and many plant species. Previous research has shown that pretreatment of citrus leaves with Xanthomonas citri subsp. citri (Xcc), which causes citrus canker, significantly improves the AMTE efficacy. Here, we have shown that Xcc promotes AMTE mainly through triggering cell division and upregulating plant cell wall-degrading enzymes. We demonstrate that Xcc improves AMTE via PthA, a transcription activator-like effector known to trigger cell division in citrus, and mutation of pthA4 abolished the promoting effect of Xcc. Mutation of the effector (PthA4)-binding element in the promoter region and coding region of CsLOB1, which is known to be directly activated by PthA4, significantly reduced Xcc promotion of AMTE. Mutation of PthA4 significantly reduced the expression of cell division-related genes (CDKA, CDKB1-2, and CDKB2-2) compared with wild-type Xcc and the complemented strain. Cell division inhibitor mimosine but not colchicine also significantly decreased Xcc promotion of AMTE. In addition, PthA4 is known to upregulate plant growth hormones auxin (indole-3-acetic acid), gibberellin, and cytokinin, as well as cell wall-degrading enzymes (e.g., cellulase). Exogenous application of indole-3-acetic acid, cytokinin, and cellulase but not gibberellin significantly improved AMTE in leaves of sweet orange, pummelo, Meiwa kumquat, lucky bamboo, and rose mallow. Our study provides a mechanistic understanding of how Xcc promotes AMTE and develops practical measures to improve AMTE via pretreatment with plant hormones (i.e., auxin and cytokinin) and cellulase. [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.

Host-protective or disease-suppressive microorganisms are emerging as sustainable solutions for controlling crop diseases, such as bacterial wilt. However, the efficacy of biocontrol strategies is often constrained by limited resilience under varying environmental conditions and interactions with native microbial communities in the field. One major challenge is that introduced biocontrol microbes often face suppression by indigenous microbes due to competitive interactions. Synthetic communities (SynComs) offer a promising alternative strategy. However, conventional approaches to assembling SynComs by combining different microbial isolates often result in antagonism and competition among strains, leading to ineffective and inconsistent outcomes. In this study, we assembled a bacterial wilt-suppressive SynCom for tomato, composed of bacterial isolates derived from co-cultured microbial complexes associated with healthy plants. This SynCom demonstrates significant disease-suppressive effects against Ralstonia pseudosolanacearum in tomato seedlings under both axenic and soil conditions. Additionally, our findings suggest the presence of an optimal SynCom colonization level in plants, which is crucial for effective disease suppression. The SynCom also exhibits direct antibiotic activity and modulates the plant-associated microbiome. Our results provide an effective approach to constructing SynComs with consistent and effective disease-suppressive properties within microbial community contexts. [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.