Plant diseases caused by diverse phytopathogens persistently threaten global food security and agricultural sustainability. Conventional resistance breeding is limited by a scarcity of broad-spectrum resistance genes and the frequent breakdown of race-specific resistance under field conditions. Meanwhile, the reliance on chemical pesticides raises environmental and human health concerns, creating an urgent need for green and effective disease management strategies. Beneficial microorganisms, including plant growth-promoting rhizobacteria, mycorrhizal fungi, and endophytes, offer a promising solution by their excellent function in eliciting broad-spectrum resistance in various crops. Recent advances have moved beyond traditional mechanisms such as direct antagonism or induced systemic resistance (ISR) alone. A key conceptual breakthrough is the recognition that microbial effectors, which have been most studied in the context of pathogenesis, also play essential roles in beneficial plant-microbe interactions. These secreted molecules have been shown to suppress local immune responses to facilitate initial colonization, reprogram plant primary and secondary metabolism, and activate longlasting systemic immunity without causing detrimental growth defense tradeoffs. Understanding this effector-driven dialogue has opened new avenues and laid a foundation for exploring new resistance gene resources and eventually engineering broad-spectrum resistance. Building on these insights, two complementary effector-based strategies are currently being developed. The first approach aims to identify central regulatory hub proteins that govern plant immunity by dissecting how specific beneficial effectors activate immune networks. Such hubs can serve as precise targets for gene editing to create crop germplasm with durable, broad-spectrum resistance. The second strategy uses characterized effectors as molecular probes to screen microbial communities associated with healthy plants. This enables rapid isolation of highly efficient beneficial strains with strong immune-eliciting activities, which can then be formulated into bioinoculants or synthetic microbial consortia for field application. Beyond effector-based engineering, current application-oriented efforts focus on synthetic consortia (SynComs) that combine complementary strains to enhance stability and broad-spectrum efficacy. Another focus is the exploitation of microbial antimicrobial compounds, particularly proteins that can be directly applied as biopesticides. However, careful considerations regarding purity, strain safety, dosage, environmental factors, and minimal impact on beneficial microbiota are essential to avoid the development of resistance in phytopathogens. Elucidating the effector-driven dialogue, together with advancing SynCom design and antimicrobial compound discovery, will accelerate sustainable crop protection. Future disease management lies in translating these insights into microbial products and precision breeding, integrated with agronomic practices such as precision irrigation, cover cropping, and straw return. High-throughput screening and modeling to optimize strain crop environment matching will be critical for efficient field application.

Late blight, caused by oomycete pathogen Phytophthora infestans, is one of the most devastating diseases of potato and tomato. Plant resistance to pathogens relies on a sophisticated innate immune system, which is often targeted by pathogen-derived effectors. P. infestans secretes numerous RXLR effectors to suppress host immunity. In this study, we show that the P. infestans core effector Pi05910 functions as a virulence factor and targets the host scaffold protein Receptor for Activated C Kinase 1 (RACK1), which is identified to positively regulate potato resistance to late blight. Functional analyses showed that StRACK1-silencing in potato, and tobacco rattle virus (TRV)-based virus-induced NbRACK1-silencing in Nicotiana benthamiana, consistently increased host susceptibility to P. infestans colonisation, whereas transient expression of NbRACK1 in N. benthamiana or stable overexpression of StRACK1 in potato enhanced late blight resistance. Pi05910 physically interacts with RACK1 and promotes its destabilisation via the host 26S proteasome pathway. The destabilisation of RACK1 led to the inhibition of PAMP elicitor INF1-triggered plant immune responses, including reactive oxygen species burst and expression of defence-related genes such as StWRKY7 and StWRKY8, and suppression of potato and N. benthamiana growth and global protein translation. Our findings reveal a strategy whereby a pathogen effector sabotages a key potato immune scaffold StRACK1 to promote plant susceptibility to P. infestans infection, providing new insight into mechanisms of effector-triggered plant susceptibility.

Context and problem: As potato is one of the four major food crops, enhancing yield is crucial, particularly when considering the mitigation of environmental impacts. Deep fertilization represents a potential strategy for efficient nutrient utilization; however, its specific on potato yield, quality and greenhouse gas emissions require further elucidation. Methods: We conducted a four-year field experiment (2020-2023) using potatoes as the test crop. We investigated the impacts of four fertilization depths (D5, 5 cm, control with locally conventional fertilization depth; D15, 15 cm; D25, 25 cm; D35, 35 cm) on soil C, N, and P content and ratios, enzyme activity, greenhouse gas emissions, potato growth, yield, and quality. Results: Deep fertilization significantly increased the soil SOC:TN, SOC:TP, MBC:MBN, and SIC:SIN ratios, while decreasing the MBC:MBP, MBN:MBP, and POC:PON ratios. In addition to soil catalase, the activities of invertase, urease and phosphatase were closely related to the soil C:N:P ratio. Specifically, deep fertilization increased soil invertase and phosphatase activities but decreased catalase and urease activities. Correlation analysis showed that N2O and CO2 emissions were positively correlated with soil urease activity, whereas CH4 uptake and CO2 emissions were negatively correlated with soil phosphatase and sucrase activities, respectively. Furthermore, increase of soil phosphatase activity enhanced the leaf area index, net photosynthetic rate, and dry matter accumulation of potato while reducing stem lodging, ultimately improving yield and quality. Among these treatments, D25 achieved the highest improvements in large potato rate (16.4 %) and yield (11.5 %), while simultaneously resulting in high tuber quality in starch (42.5 %), reducing sugar (52.7 %), protein (33.4 %), and vitamin C (31.9 %) content. In addition, its greenhouse gas emission intensity was also at the lowest level (decreased by 32.7 %). Conclusions: Deep fertilization affects enzyme activity by altering soil C:N:P ratios, thereby promoting potato production and reducing greenhouse gas emissions. In this region, fertilization depths of 15-25 cm exhibited distinct advantage in terms of yield enhancement, whereas depths exceeding 35 cm were more effective in reducing emissions.

[This corrects the article DOI: 10.3389/fpls.2020.00919.].

The symbiotic fungus Serendipita indica confers broad-spectrum beneficial effects on diverse plant hosts. Its key effector SIE141 elicits immunity against Phytophthora and salt tolerance by binding and relocalizing thioredoxin CDSP32 from chloroplast to the nucleus. Here, we show that this functionally essential nuclear transfer process of the SIE141-CDSP32 complex is mediated by the host NTF2 proteins. NTF2 family proteins are direct targets of SIE141, whose knockdown abolished nuclear accumulation of both SIE141 and CDSP32, leading to their rendered accumulation to chloroplasts. The glutamine residue at position 40 of NbNTF2A is critical for its interaction with both SIE141 and Ran GTPase 1. SIE141 modulates NbNTF2-NbRan1 interaction in a dose-dependent manner, without impairing nuclear accumulation of NbRan1 and the NTF2-mediated positive immune function of Ran1. Our results reveal a previously unknown mechanism where a beneficial symbiotic fungal effector utilizes the conserved NTF2 rather than other core nuclear import machinery components to traffic an immune complex and enhance disease resistance. These findings provide a potential strategy for engineering plant immunity by manipulating NTF2-RanGTPase dependent nucleocytoplasmic transport.

Climate change has intensified the randomness of precipitation events, threatening the production stability of rainfed agricultural regions. The addition of biochar with a suitable particle size can effectively mitigate these adverse impacts. In this study, biochar of three particle sizes (SB, small: <0.5 mm; MB, moderate: 0.5-2.0 mm; and LB, large: >2.0 mm) were added to typical rainfed farmland to investigate its effects on potato source-sink relationships, yield, precipitation use efficiency (PUE), nitrogen use efficiency (NUE), soil micro-environment (NO3--N and NH4+-N contents, oxygen concentration, temperature, water-filled pore space), N2O emissions, and nitrogen leaching under varied precipitation patterns. Potato tuber yield was mainly governed by precipitation distribution, with biochar addition exerting a secondary effect. By contrast, biochar addition primarily reduced soil N2O emissions, and this mitigating effect was enhanced with increasing precipitation. The application of small and moderate particle size biochar under different precipitation patterns significantly improved the soil micro-environment, and promoted potato source-sink activity and assimilate demand. Among these treatments, MB achieved the best comprehensive effects, it significantly increased tuber yield, PUE, and NUE by 17.8 %, 17.1 %, and 60.8 %, respectively, while lowering soil N2O emissions, yield-scaled N2O emissions, and nitrogen leaching by 29.8 %, 40.2 %, and 20.6 %, respectively. In comparison, LB did not only fail to significantly increase tuber yield but also increased nitrogen leaching. Therefore, added biochar with a particle size of 0.5-2.0 mm can support sustainable potato production in Northwest China.

Context: Nitrogen management is pivotal for attaining sustainable agricultural development in the future. Among the array of mitigation strategies, deep fertilization emerges as a promising approach to address the multifaceted challenges associated with agricultural productivity, environmental sustainability, economic efficiency, and social demands. Objective: This study seeks to comprehensively assess the effects of deep nitrogen fertilization on potato productivity, environmental footprint, ecological and social costs and benefits. The findings are Intended to provide furnish an actionable guidance for advancing sustainable potato production in Northwest China. Methods: Field experiments were conducted over three consecutive years (2021-2023) at four representative sites spanning two typical climatic zones in Northwest China: the arid region (Ganzhou and Yongchang-Site 1 and Site 2) and the semi-arid region (Anding and Jingning-Site 3 and Site 4). All trials were integrated into local mainstream potato cultivation practices, with drip irrigation applied at Sites 1, 2, and 3, whereas Site 4 was cultivated under rain-fed cultivations. Four nitrogen fertilization depths were investigated: D5 (5 cm), D15 (15 cm), D25 (25 cm), and D35 (35 cm), to assess the effects of nitrogen placement depth on multiple performance indicators. Results: In arid region, the lowest nitrogen footprint (NF) and carbon footprint (CF), as well as the highest yield, N-derived potato tuber yield (YN), N-Partial factor productivity (PFPN), private profitability (BP), ecological benefits (BE) and social benefits (BS) were observed when the fertilization depth was 15 cm, while the best performance was observed at 25 cm in semi-arid region. In addition, when the fertilization depth is 35 cm, the ecological cost (Ecost) and social cost (Scost) in arid and semi-arid regions are the lowest. Compared with the conventional fertilization depth (D5) in the northwest region, the NF, CF, Ecost and Scost were significantly reduced by 14.8-34.2 %, 7.1-20.6 %, 15.0-19.7 % and 20.1-25.1 % when the optimal treatment depth was adjusted, and the yield, YN, PFPN, BP, BE and BS were significantly increased by 4.7-22.2 %, 10.2-42.8 %, 4.7-22.2 %, 10.4-86.7 %, 10.9-88.4 % and 11.8-92.5 %. The regression analysis revealed a clear spatial pattern: the optimal fertilization depth for maximizing productivity, minimizing environmental footprint, optimizing cost and benefit was generally shallower in arid areas compared to the semi-arid area, and shallower in the drip irrigation area than in the rain-fed area (with the exception of cost). Conclusions: Based on the comprehensive evaluation of productivity, environmental impacts, and economic and social outcomes, we recommend adjusting the fertilization depths to approximately 18.0 cm for Site 1, 13.3 cm for Site 2, 20.2 cm for Site 3, and 22.9 cm for Site 4. These adjustments are expected to enhance potato pro-ductivity and overall benefits.

Late blight pathogen Phytophthora infestans secretes numerous effectors to suppress plant immunity. However, little is known about their underlying biochemical mechanisms. Here we report that, in the host Nicotiana benthamiana, P. infestans core RXLR effector Pi17063 suppresses plant immunity by targeting the host plasma membrane and NbRab-G3 proteins, small GTPases of the Ras-related brain (Rab) family. Pi17063 functions as their specific GTPase-activating protein (GAP), driving them to the cytoplasm-localized guanosine diphosphate (GDP)-bound inactive state. Mutant analysis of the conserved Pi17063 arginine residues showed the essential role of its GAP activity for virulence contribution. All four NbRab-G3 subfamily members are positive immune regulators, and NbRab-G3c mutants lost the ability to switch between active and inactive states and showed compromised immune function. Consistent with this, both silencing and overexpression of an endogenous GAP, NbGYP, inhibited NbRab-G3c-mediated plant immunity. Our results revealed positive immune roles of host NbRab-G3 GTPases, the importance of their state balance, and the biochemical mechanism by which their functions are suppressed by a P. infestans effector, providing insights into understanding eukaryotic effector-mediated plant susceptibility.

Reactive oxygen species (ROS) are key signaling molecules in plant development and immunity, but current understanding is primarily focused on apoplastic and chloroplastic ROS. Mitochondria are also a key source of intracellular ROS, yet their contribution to plant immunity is poorly characterized. Here, we studied mitochondrial ROS (mROS) function in plant-pathogen interactions, deploying genetically encoded sensors, assorted fluorescent markers, and genetic approaches to track mROS, specifically H2O2, dynamics and identify interorganelle contact sites. We unexpectedly found a mitochondria-endoplasmic reticulum (ER) ROS signal cascade functioning independently of apoplastic and chloroplastic ROS in plant immunity. mROS initiate immune responses induced by the oomycete pathogen Phytophthora parasitica and promote mitochondria-ER association. These enhanced mitochondria-ER membrane associations are required for transfer of mROS signals and initiation of extensive unfolded protein responses. We conclude that mROS transfer via mitochondria-ER membranes to the ER lumen is an underappreciated yet essential component in plant defense.

Papain-like cysteine proteases (PLCPs) are pivotal in plant development and immunity, though their specific regulatory mechanisms in immune responses remain largely unexplored. In this study, we identify AtRD19C, a vacuole-localized PLCP, and demonstrate its role in negatively regulating plant immunity to Phytophthora parasitica. We show that AtRD19C suppresses the ethylene (ET) signaling pathway by destabilizing the copper chaperone AtATX1, which is essential for activating ET signaling through the ethylene receptor ETR1. Genetic and biochemical analyses reveal that AtATX1 and the ET signaling pathway positively regulate immunity against Phytophthora. Given the conserved roles of RD19C and ATX1 in Solanum tuberosum, our findings suggest a conserved mechanism by which RD19C and ATX1 regulate resistance to Phytophthora across plant species.

Phytophthora species are oomycetes that cause significant losses in agricultural production and damages to natural ecosystems. Phytophthora pathogens secrete numerous cytoplasmic effectors that target distinct cellular components to suppress host immunity and facilitate pathogen colonisation. The identification of their host targets is crucial for deciphering the mechanisms they employ to modulate host immunity. Here, we found that multiple Phytophthora Avr3a-like effectors interact with host plant cinnamyl alcohol dehydrogenase CAD5, as revealed by yeast two-hybrid and co-immunoprecipitation assays. Analysis of Arabidopsis thaliana T-DNA insertion mutants and overexpression lines, as well as analysis of RNA silencing Nicotiana benthamiana plants, showed that CAD5 positively regulates plant immunity to Phytophthora pathogens. Overexpression and silencing analyses showed that CAD5 plays a positive role in plant PAMP-triggered immunity (PTI) responses, including enhanced callose deposition, promoted cell death induced by INF1, and in plant effector-triggered immunity (ETI) responses mediated by R3a/PiAvr3aKI recognition. CAD5 enzymatic activity was inhibited by Avr3a-like effectors, and mutagenesis analyses showed its crucial role in the positive regulation of plant immunity. In conclusion, our research showed that the Phytophthora Avr3a-like effectors target the conserved immune regulator CAD5 and suppress its enzymatic activity, which is required for both plant PTI and ETI responses.

RXLR effectors secreted by Phytophthora pathogens are important virulence factors in suppressing plant immunity and facilitating pathogen infection. In addition to possessing a variety of functions, some RXLR effectors have been found to trigger host cell death with different underlying mechanisms. PpE4 was previously reported as a virulent RXLR effector secreted by Phytophthora parasitica and triggers cell death in various plants. However, it is uncertain whether this type of cell death promotes or restricts the colonization of this hemibiotrophic pathogen. Here, we explored the correlation between the cell death activity of PpE4 and its contribution to the infection of P. parasitica. Sequencing data revealed that PpE4 exhibited both point mutations and presence/absence polymorphisms in the P. parasitica population under positive selection. E4D, one of four alleles, lost its cell death-inducing ability, also lost its ability to increase plant susceptibility to pathogen infection. Furthermore, E4D could compromise the cell death-inducing and virulence functions of the other three PpE4 alleles. PpE4 truncated mutants deficient in cell death-inducing activity showed abolished ability to increase plant susceptibility. Finally, PpE4 was unable to increase the susceptibility of TRV-NPK plants, which showed abolished cell death. Taken together, the cell death-inducing activity of PpE4 is essential for its virulence function during colonization of hemibiotrophic pathogen, suggesting that P. parasitica exploits the cell death triggered by PpE4 to facilitate the transition from biotrophy to necrotrophy. These findings provide a new perspective for understanding the role of RXLR effectors triggered cell death in the pathogenesis of hemibiotrophic pathogens.

Late blight, caused by the oomycete Phytophthora infestans, is one of the most destructive diseases affecting potato production globally. However, the function of DNA methylation (DNAm) and its association with simultaneous alteration in gene expression in potato's response to P. infestans infection remain largely unknown. Here, we conducted whole-genome bisulfite sequencing and RNA sequencing on potato cultivar Qingshu No.9 inoculated with P. infestans. Significantly, we identified 18 119 differentially expressed genes (DEGs) across at least one of the four post-inoculation time points. A few pathogenesis-related (PR) genes involved in salicylic acid, ethylene signaling, and DNAm regulation exhibited activation at early infection stages, although they were predominantly downregulated after the onset of necrosis in plants. Hypomethylation changes at 12 h post-inoculation (hpi) were followed by hypermethylation at 24 hpi, with CHH methylation being the primary factor influencing the DNAm pattern. Differentially methylated regions (DMRs) showed significant enrichment at DEGs. Specially, DNAm variations could be associated with subsequent transcriptional changes. This is exemplified by 24 h-hyper-CHG methylation at the gene body that correlates with expression downregulation at 48 hpi, including genes involved in chromatin remodeling pathways. Furthermore, we observed a significant enrichment of hypomethylation changes at the exon of NB-LRR genes, which ultimately resulted in their downregulation. In summary, we have elucidated the DNAm pattern of potato in response to infection by P. infestans, and identified the involvement of epigenetic mechanisms in the reprogramming of the transcriptome, which ultimately contributed to the suppression of immunity and the development of potato late blight.

Negative immune regulator CAD7 is a non-canonical member of the CAD (cinnamyl alcohol dehydrogenase) family in plants. However, little is known on its biochemical functions and underlying mechanisms of immune regulation. Here, we show that Arabidopsis thaliana AtCAD7 harbours substrate-binding residues divergent from lignin-forming CADs (AtCAD4/5), being conserved with bacterial alcohol dehydrogenases EcYahK and EcYjgB. Comparative enzymatic analysis revealed that AtCAD7 exhibits a broad substrate preference for diverse small-molecule aldehydes, including histamine-derived intermediates, being distinct from the canonical lignin-forming AtCAD5. Metabolomic analyses revealed that AtCAD7-overexpression transformants were affected in the biosynthesis and metabolism of amino acids, whereas AtCAD7-silencing lines were activated in the phenylpropanoid pathway and increased in flavonoid accumulation. Histamine was elevated in AtCAD7-overexpression lines and functional validation revealed its promoted effect on plant susceptibility to Phytophthora parasitica. In contrast, phytoalexins scopolin and chlorogenic acid were enriched in AtCAD7-silencing lines, accompanied by upregulated expression of phenylpropanoid pathway-related genes. Functional validation demonstrated that scopolin and chlorogenic acid enhanced plant resistance to P. parasitica. Collectively, our study uncovers that CAD7 functions as a metabolic hub linking small-molecule aldehyde reductase activity to immune suppression, providing a potential novel target for developing crops with enhanced resistance to Phytophthora pathogens.

Phytophthora infestans is a destructive oomycete that causes the late blight of potato and tomato worldwide. It secretes numerous small proteins called effectors in order to manipulate host cell components and suppress plant immunity. Identifying the targets of these effectors is crucial for understanding P. infestans pathogenesis and host plant immunity. In this study, we show that the virulence RXLR effector Pi23014 of P. infestans targets the host nucleus and chloroplasts. By using a liquid chromatogrpahy-tandem mass spectrometry assay and co-immunoprecipitation assasys, we show that it interacts with NbRBP3a, a putative glycine-rich RNA-binding protein. We confirmed the co-localization of Pi23014 and NbRBP3a within the nucleus, by using bimolecular fluorescence complementation. Reverse transcription-quantitative PCR assays showed that the expression of NbRBP3a was induced in Nicotiana benthamiana during P. infestans infection and the expression of marker genes for multiple defence pathways were significantly down-regulated in NbRBP3-silenced plants compared with GFP-silenced plants. Agrobacterium tumefaciens-mediated transient overexpression of NbRBP3a significantly enhanced plant resistance to P. infestans. Mutations in the N-terminus RNA recognition motif (RRM) of NbRBP3a abolished its interaction with Pi23014 and eliminated its capability to enhance plant resistance to leaf colonization by P. infestans. We further showed that silencing NbRBP3 reduced photosystem II activity, reduced host photosynthetic efficiency, attenuated Pi23014-mediated suppression of cell death triggered by P. infestans pathogen-associated molecular pattern elicitor INF1, and suppressed plant immunity.

Small RNAs are involved in diverse cellular processes, including plant immunity to pathogens. Here, we report that miR158a negatively regulates plant immunity to the oomycete pathogen Phytophthora parasitica in Arabidopsis thaliana. By performing real-time quantitative PCR, transient expression, and RNA ligase-mediated 5 ' rapid amplification of cDNA ends assays, we demonstrate that miR158a downregulates AtTN7 expression by cleaving its 3 '-untranslated region. AtTN7 positively affects plant immunity and encodes a truncated intracellular nucleotide-binding site and leucine-rich repeat receptor containing the Toll/interleukin-1 receptor. AtTN7 can degrade oxidized forms of nicotinamide adenine dinucleotide (NAD+). Further genetic and molecular analyses reveal that the Enhanced Disease Susceptibility 1-Phytoalexin Deficient 4-Activated Disease Resistance 1 complex is required for AtTN7-mediated immunity. ADR1-dependent Ca2+ influx is crucial for activating salicylic acid signaling to condition AtTN7-triggered immunity. Our study uncovers the immune roles and regulatory mechanisms of miR158a and its target AtTN7. Both miR158a-downregulation and AtTN7-overexpression lead to enhanced plant resistance to P. parasitica without affecting plant growth phenotypes, suggesting their application potentials and the utilization of miRNAs in identifying novel immune genes for the development of plant germplasm resources with enhanced disease resistance.

Phytophthora parasitica causes diseases on a broad range of host plants. It secretes numerous effectors to suppress plant immunity. However, only a few virulence effectors in P. parasitica have been characterized. Here, we highlight that PpE18, a conserved RXLR effector in P. parasitica, was a virulence factor and suppresses Nicotiana benthamiana immunity. Utilizing luciferase complementation, co-immunoprecipitation, and GST pull-down assays, we determined that PpE18 targeted NbAPX3-1, a peroxisome membrane-associated ascorbate peroxidase with reactive oxygen species (ROS)-scavenging activity and positively regulates plant immunity in N. benthamiana. We show that the ROS-scavenging activity of NbAPX3-1 was critical for its immune function and was hindered by the binding of PpE18. The interaction between PpE18 and NbAPX3-1 resulted in an elevation of ROS levels in the peroxisome. Moreover, we discovered that the ankyrin repeat-containing protein NbANKr2 acted as a positive immune regulator, interacting with both NbAPX3-1 and PpE18. NbANKr2 was required for NbAPX3-1-mediated disease resistance. PpE18 competitively interfered with the interaction between NbAPX3-1 and NbANKr2, thereby weakening plant resistance. Our results reveal an effective counter-defense mechanism by which P. parasitica employed effector PpE18 to suppress host cellular defense, by suppressing biochemical activity and disturbing immune function of NbAPX3-1 during infection.

Phytophthora infestans is a notorious oomycete pathogen that causes potato late blight. It secretes numerous effector proteins to manipulate host immunity. Understanding mechanisms underlying their host cell manipulation is crucial for developing disease resistance strategies. Here, we report that the conserved RXLR effector Pi05910 of P. infestans is a genotype-specific avirulence elicitor on potato variety Longshu 12 and contributes virulence by suppressing and destabilizing host glycolate oxidase StGOX4. By performing co-immunoprecipitation, yeast-two-hybrid assays, luciferase complementation imaging, bimolecular fluorescence complementation and isothermal titration calorimetry assays, we identified and confirmed potato StGOX4 as a target of Pi05910. Further analysis revealed that StGOX4 and its homologue NbGOX4 are positive immune regulators against P. infestans, as indicated by infection assays on potato and Nicotiana benthamiana overexpressing StGOX4 and TRV-NbGOX4 plants. StGOX4-mediated disease resistance involves enhanced reactive oxygen species accumulation and activated the salicylic acid signalling pathway. Pi05910 binding inhibited enzymatic activity and destabilized StGOX4. Furthermore, mutagenesis analyses indicated that the 25th residue (tyrosine, Y25) of StGOX4 mediates Pi05910 binding and is required for its immune function. Our results revealed that the core RXLR effector of P. infestans Pi05910 suppresses plant immunity by targeting StGOX4, which results in decreased enzymatic activity and protein accumulation, leading to enhanced plant susceptibility.

The root endophytic fungus Serendipita indica establishes beneficial symbioses with a broad spectrum of plants and enhances host resilience against biotic and abiotic stresses. However, little is known about the mechanisms underlying S. indica-mediated plant protection. Here, we report S. indica effector (SIE) 141 and its host target CDSP32, a conserved thioredoxin-like protein, and underlying mechanisms for enhancing pathogen resistance and abiotic salt tolerance in Arabidopsis thaliana . SIE141 binding interfered with canonical targeting of CDSP32 to chloroplasts, leading to its re-location into the plant nucleus. This nuclear translocation is essential for both their interaction and resistance function. Furthermore, SIE141 enhanced oxidoreductase activity of CDSP32, leading to CDSP32-mediated monomerization and activation of NONEXPRESSOR OF PATHOGENESIS-RELATED 1 (NPR1), a key regulator of systemic resistance. Our findings provide functional insights on how S. indica transfers well-known beneficial effects to host plants and indicate CDSP32 as a genetic resource to improve plant resilience to abiotic and biotic stresses.

Phytophthora parasitica is a highly destructive oomycete plant pathogen that is capable of infecting a wide range of hosts including many agricultural cash crops, fruit trees, and ornamental garden plants. One of the most important diseases caused by P. parasitica worldwide is black shank of tobacco. Rapid, sensitive, and specific pathogen detection is crucial for early rapid diagnosis, which can facilitate effective disease management. In this study, we used a genomics approach to identify repeated sequences in the genome of P. parasitica by genome sequence alignment and identified a 203-bp P. parasitica-specific sequence, PpM34, that is present in 31 to 60 copies in the genome. The P. parasitica genome specificity of PpM34 was supported by PCR amplification of 24 genetically diverse strains of P. parasitica, 32 strains representing 12 other Phytophthora species, one Pythium species, six fungal species, and three bacterial species, all of which are plant pathogens. Our PCR and real-time PCR assays showed that the PpM34 sequence was highly sensitive in specifically detecting P. parasitica. Finally, we developed a PpM34-based high-efficiency recombinase polymerase amplification assay, which allowed us to specifically detect as little as 1 pg of P. parasitica total DNA from both pure cultures and infected Nicotiana benthamiana at 39°C using a fluorometric thermal cycler. The sensitivity, specificity, convenience, and rapidity of this assay represent a major improvement for early diagnosis of P. parasitica infection.