Confer Disease Resistance Research Articles

Mutation in Bruton Tyrosine Kinase (BTK) A428D confers resistance To BTK-degrader therapy in chronic lymphocytic leukemia

Targeting BTK has profoundly changed the face of CLL treatment over the past decade. Iterative advances in the cat and mouse game of resistance and redesign have moved BTK inhibitors from covalent to non-covalent and now targeted protein degraders. However, contrary to the presumption that protein degraders may be impervious to mutations in BTK, we now present clinical evidence that a mutation in the kinase domain of BTK, namely A428D, can confer disease resistance to a BTK degrader currently in clinical trials, that is BGB-16673. Modeling of a BTK A428D mutation places a negatively charged aspartic acid in place of the hydrophobic side chain of alanine within the binding pocket of another BTK-degrader in clinical development, namely NX-2127, suggesting that CLL cells with BTK A428D also may be resistant to NX-2127, as they already are known to be with either non-covalent or covalent inhibitors of BTK. Consequently, the two BTK degraders furthest advanced in clinical trials potentially may select for CLL cells with BTK A428D that are resistant to all approved BTKi’s.

Comparative analysis on natural variants of fire blight resistance protein FB_MR5 indicates distinct effector recognition mechanisms

FB_MR5 is an NLR protein identified from wild apple species Malus × robusta 5 conferring disease resistance to bacterial fire blight. FB_MR5 (hereafter MrMR5) recognizes the cysteine protease effector EaAvrRpt2 secreted from the causal agent of bacterial fire blight, Erwinia amylovora. We previously reported that MrMR5 is activated by the C-terminal cleavage product (ACP3) of Malus domestica RIN4 (MdRIN4) produced by EaAvrRpt2-directed proteolysis. Here, we show that MbMR5 from a wild apple species Malus baccata share 99.4% amino acid sequence identity with MrMR5. Surprisingly, transient expression of MbMR5 in Nicotiana benthamiana showed auto-activity in contrast to MrMR5. Domain swap and mutational analyses revealed that one amino acid polymorphism in the MbMR5 CC domain is critical in enhancing auto-activity. We further demonstrated that MrMR5 carrying seven amino acid polymorphisms present in MbMR5 is not activated by MdRIN4 ACP3 but recognizes AvrRpt2 without MdRIN4 in Nicotiana benthamiana. Our findings indicate that naturally occurring polymorphisms of MR5 natural variants can confer its cell death-inducing activity and the effector recognition mechanism likely due to altered compatibility with RIN4.

The Identification of the Peanut Wild Relative Arachis stenosperma as a Source of Resistance to Stem Rot and Analyses of Genomic Regions Conferring Disease Resistance through QTL Mapping

Peanut stem rot, also known as white mold, poses a significant threat to peanut production. It is typically managed using fungicides and moderately resistant cultivars. Cultivars with higher resistance can reduce fungicide dependency and increase sustainability. This study explores the potential of wild peanut species in stem rot resistance breeding programs by enhancing genetic diversity in cultivated peanut. Through greenhouse and field evaluations, 13 allotetraploid hybrids with Arachis stenosperma as one of the parents showed superior resistance compared to other wild genotypes. The genomic regions that confer the stem rot resistance were further identified by genotyping and phenotyping an F2 population derived from the allotetraploid ValSten1 (A. valida × A. stenosperma)4× and A. hypogaea cv. TifGP-2. A linkage map was constructed from 1926 SNP markers. QTL analysis revealed both beneficial and deleterious loci, with two resistance-associated QTLs derived from A. stenosperma and four susceptibility loci, two from A. stenosperma and two from A. valida. This is the first study that evaluated peanut-compatible wild-derived allotetraploids for stem rot resistance and that identified wild-derived QTLs for resistance to this pathogen. The allotetraploid hybrid ValSten1, that has A. stenosperma as one of the parents, offers a resource for resistance breeding. Markers associated with resistance QTLs can facilitate introgression from ValSten1 into cultivated peanut varieties in future breeding efforts, potentially reducing reliance on chemical control measures.

The miR7125‐MdARF1 module enhances the resistance of apple to Colletotrichum gloeosporioides by promoting lignin synthesis in response to salicylic acid signalling

SummaryApple is an important cash crop in China, and it is susceptible to fungal infections that have deleterious effects on its yield. Apple bitter rot caused by Colletorichum gloeosporioides is one of the most severe fungal diseases of apple. Salicylic acid (SA) is a key signalling molecule in the plant disease resistance signalling pathways. Lignin synthesis also plays a key role in conferring disease resistance. However, few studies have clarified the relationship between the SA disease resistance signalling pathway and the lignin disease resistance pathway in apple. MdMYB46 has previously been shown to promote lignin accumulation in apple and enhance salt and osmotic stress tolerance. Here, we investigated the relationship between MdMYB46 and biological stress; we found that MdMYB46 overexpression enhances the resistance of apple to C. gloeosporioides. We also identified MdARF1, a transcription factor upstream of MdMYB46, via yeast library screening and determined that MdARF1 was regulated by miR7125 through psRNATarget prediction. This regulatory relationship was confirmed through LUC and qRT‐PCR experiments, demonstrating that miR7125 negatively regulates MdARF1. Analysis of the miR7125 promoter revealed that miR7125 responds to SA signals. The accumulation of SA level will result in the decrease of miR7125 expression level. In sum, the results of our study provide novel insights into the molecular mechanisms underlying the resistance of apple to C. gloeosporioides and reveal a new pathway that enhances lignin accumulation in apple in response to SA signals. These findings provide valuable information for future studies aimed at breeding apple for disease resistance.

Plant triterpenoid saponins function as susceptibility factors to promote the pathogenicity of Botrytis cinerea

The gray mold fungus Botrytis cinerea is a necrotrophic pathogen that causes diseases in hundreds of plant species, including high-value crops. Its polyxenous nature and pathogenic success are due to its ability to perceive host signals in its favor. In this study, we found that laticifer cells of Euphorbia lathyris are a source of susceptibility factors required by B. cinerea to cause disease. Consequently, poor-in-latex (pil) mutants, which lack laticifer cells, show full resistance to this pathogen, whereas lot-of-latex mutants, which produce more laticifer cells, are hypersusceptible. These S factors are triterpenoid saponins, which are widely distributed natural products of vast structural diversity. The downregulation of laticifer-specific oxydosqualene cyclase genes, which encode the first committed step enzymes for triterpene and, therefore, saponin biosynthesis, conferred disease resistance to B. cinerea. Likewise, the Medicago truncatula lha-1 mutant, compromised in triterpenoid saponin biosynthesis, showed enhanced resistance. Interestingly, the application of different purified triterpenoid saponins pharmacologically complemented the disease-resistant phenotype of pil and hla-1 mutants and enhanced disease susceptibility in different plant species. We found that triterpenoid saponins function as plant cues that signal transcriptional reprogramming in B. cinerea, leading to a change in its growth habit and infection strategy, culminating in the abundant formation of infection cushions, the multicellular appressoria apparatus dedicated to plant penetration and biomass destruction in B. cinerea. Taken together, these results provide an explanation for how plant triterpenoid saponins function as disease susceptibility factors to promote B. cinerea pathogenicity.

Ectopic Expression of the Executor-Type R Gene Paralog Xa27B in Rice Leads to Spontaneous Lesions and Enhanced Disease Resistance.

Plant disease resistance (R) gene-mediated effector-triggered immunity (ETI) is usually associated with hypersensitive response (HR) and provides robust and race-specific disease resistance against pathogenic infection. The activation of ETI and HR in plants is strictly regulated, and improper activation will lead to cell death. Xa27 is an executor-type R gene in rice induced by the TAL effector AvrXa27 and confers disease resistance to Xanthomonas oryzae pv. oryzae (Xoo). Here we reported the characterization of a transgenic line with lesion mimic phenotype, designated as Spotted leaf and resistance 1 (Slr1), which was derived from rice transformation with a genomic subclone located 5,125 bp downstream of the Xa27 gene. Slr1 develops spontaneous lesions on its leaves caused by cell death and confers disease resistance to both Xoo and Xanthomonas oryzae pv. oryzicola. Further investigation revealed that the Slr1 phenotype resulted from the ectopic expression of an Xa27 paralog gene, designated as Xa27B, in the inserted DNA fragment at the Slr1 locus driven by a truncated CaMV35Sx2 promoter in reverse orientation. Disease evaluation of IRBB27, IR24, and Xa27B mutants with Xoo strains expressing dTALE-Xa27B confirmed that Xa27B is a functional executor-type R gene. The functional XA27B-GFP protein was localized to the endoplasmic reticulum and apoplast. The identification of Xa27B as a new functional executor-type R gene provides additional genetic resources for studying the mechanism of executor-type R protein-mediated ETI and developing enhanced and broad-spectrum disease resistance to Xoo through promoter engineering. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Colonization compatibility with Bacillus altitudinis confers soybean seed rot resistance.

The plant microbiome and plant-associated bacteria are known to support plant health, but there are limited studies on seed and seedling microbiome to reveal how seed-associated bacteria may confer disease resistance. In this study, the application of antibiotics on soybean seedlings indicated that seed-associated bacteria were involved in the seed rot resistance against a soil-borne pathogen Calonectria ilicicola, but this resistance cannot be carried to withstand root rot. Using PacBio 16S rRNA gene full-length sequencing and microbiome analyses, 14 amplicon sequence variants (ASVs) including 2 ASVs matching to Bacillus altitudinis were found to be more abundant in the four most resistant varieties versus the four most susceptible varieties. Culture-dependent isolation obtained two B. altitudinis isolates that both exhibit antagonistic capability against six fungal pathogens. Application of B. altitudinis on the most resistant and susceptible soybean varieties revealed different colonization compatibility, and the seed rot resistance was restored in the five varieties showing higher bacterial colonization. Moreover, quantitative PCR confirmed the persistence of B. altitudinis on apical shoots till 21days post-inoculation (dpi), but 9 dpi on roots of the resistant variety TN5. As for the susceptible variety HC, the persistence of B. altitudinis was only detected before 6 dpi on both shoots and roots. The short-term colonization of B. altitudinis on roots may explain the absence of root rot resistance. Collectively, this study advances the insight of B. altitudinis conferring soybean seed rot resistance and highlights the importance of considering bacterial compatibility with plant varieties and colonization persistence on plant tissues.

Wheat dihydroflavonol-4-reductase like gene confers disease resistance by modulating NADPH pool and lignin biosynthesis

Hm1 is the first cloned disease resistance gene (R) from maize which encodes an enzyme that detoxifies Helminthosporium carbonum (HC) toxin from the fungal pathogen Cochliobolus carbonum. The homologous genes for Hm1 have been mined in various crop plants and their sequences are showed similar to dihydroflavonol-4-reductase (DFR), a key enzyme in flavonoid biosynthesis, therefore they are collectively named dihydroflavonol-4-reductase like (DFRL). The biological functions of DFRL are largely elusive. In the present study, DFRL gene was cloned from wheat, namely TaDFRL. TaDFRL was barely expressed in leaf, stem and root tissues; however, its expression level was rapidly increased following rust infection. Biochemical analysis showed that TaDFRL had the broad spectrum of substrate preference, including dihydroflavonol, flavonol and flavone, and could use both NAD and NADP as co-enzyme, which was quite distinct from DFR. Overexpressing TaDFRL in tobacco altered NAD(H) and NADP(H) pools towards to high NADPH levels. Subsequently, the gene expression of cinnamyl alcohol dehydrogenase (CAD) was up-regulated and lignin accumulation was increased. These brought about to enhance resistance to wildfire disease in tobacco plants. This research provides novel insights into DFRL mechanism, which boost host defense responses by elevating NADPH level and lignin biosynthesis.

Development of a Marker within the Candidate Un8 True Loose Smut Resistance Gene for Use in Barley Breeding

Abstract Breeding for resistance to true loose smut infection caused by the pathogen (Ustilago nuda (Jens.) Rostr.) is an economical and environmentally safe way to limit the effect of this pathogen on barley. However, screening for resistance using natural infection can lead to inconsistent results and artificial inoculation is labour intensive, and unless done in growth chambers or greenhouses, can also be affected by environmental conditions, leading to inconsistent phenotyping. Marker-assisted selection of genes conferring disease resistance can increase the efficiency of breeding programmes. A candidate gene for Un8 resistance was used to develop a genetic marker, which was tested on a recombinant inbred line (RIL) population derived from the resistant ‘CDC Freedom’ and the susceptible ‘Samson’ varieties. The RIL population (98 lines) was pheno-typed for resistance to true loose smut by artificial inoculation and genotyped with the newly developed marker. Only one of the 98 RILs tested had a resistant genotype, but was susceptible according to the artificial inoculation results. The marker was also tested in 47 additional barley cultivars and breeding material, and of the five lines with inconsistent results, four were susceptible according to the genotyping results, but were resistant according to the artificial inoculation results, while one line was resistant according to the genotyping results but had a susceptible resistance phenotype.

Recent Developments in CRISPR/Cas9 Genome-Editing Technology Related to Plant Disease Resistance and Abiotic Stress Tolerance.

The revolutionary CRISPR/Cas9 genome-editing technology has emerged as a powerful tool for plant improvement, offering unprecedented precision and efficiency in making targeted gene modifications. This powerful and practical approach to genome editing offers tremendous opportunities for crop improvement, surpassing the capabilities of conventional breeding techniques. This article provides an overview of recent advancements and challenges associated with the application of CRISPR/Cas9 in plant improvement. The potential of CRISPR/Cas9 in terms of developing crops with enhanced resistance to biotic and abiotic stresses is highlighted, with examples of genes edited to confer disease resistance, drought tolerance, salt tolerance, and cold tolerance. Here, we also discuss the importance of off-target effects and the efforts made to mitigate them, including the use of shorter single-guide RNAs and dual Cas9 nickases. Furthermore, alternative delivery methods, such as protein- and RNA-based approaches, are explored, and they could potentially avoid the integration of foreign DNA into the plant genome, thus alleviating concerns related to genetically modified organisms (GMOs). We emphasize the significance of CRISPR/Cas9 in accelerating crop breeding processes, reducing editing time and costs, and enabling the introduction of desired traits at the nucleotide level. As the field of genome editing continues to evolve, it is anticipated that CRISPR/Cas9 will remain a prominent tool for crop improvement, disease resistance, and adaptation to challenging environmental conditions.

Protein stability governed by α1-2 helices in Pvr4 is essential for localization and cell death.

Plant nucleotide-binding domain leucine-rich-repeat receptor (NLR) confers disease resistance to various pathogens by recognizing effectors derived from the pathogen. Previous studies have shown that overexpression of the CC domain in several NLRs triggers cell death, implying that the CC domain plays an important role as a signaling module. However, how CC domain transduces immune signals remains largely unknown. A Potyvirus-resistant NLR protein, Pvr4, possesses a CC domain (CCPvr4 ) that induces cell death upon transient overexpression in Nicotiana benthamiana. In this study, loss-of-function mutants were generated by error-prone PCR-based random mutagenesis to understand the molecular mechanisms underlying CCPvr4 -mediated cell death. Cell biology and biochemical studies revealed that M16 and Q52 in the α1 and α2 helices, respectively, are crucial for protein stability, and mutation of these residues disrupts localization to the plasma membrane and oligomerization activity. The increase of the protein stability of these mutants by tagging a green fluorescent protein (GFP) variant led to restoration of cell death-inducing activity and plasma membrane localization. Another mutant, I7E in the very N-terminal region, lost cell death-inducing activity by weakening the interaction with plasma membrane H+ -ATPase compared to CCPvr4 , although the protein remained in the plasma membrane. Moreover, most of the mutated residues are on the outer surface of the funnel shape in the predicted pentameric CCPvr4 , implying that the disordered N-terminal region plays a crucial role in association with PMA as well as targeting to the plasma membrane. This work could provide insights into the molecular mechanisms of cell death induced by NLR immune receptors.

Wall-associated kinase BrWAK1 confers resistance to downy mildew in Brassica rapa.

The plant cell wall is the first line of defence against physical damage and pathogen attack. Wall-associated kinase (WAK) has the ability to perceive the changes in the cell wall matrix and transform signals into the cytoplasm, being involved in plant development and the defence response. Downy mildew, caused by Hyaloperonospora brassicae, can result in a massive loss in Chinese cabbage (Brassica rapa L. ssp. pekinensis) production. Herein, we identified a candidate resistant WAK gene, BrWAK1, in a major resistant quantitative trait locus, using a double haploid population derived from resistant inbred line T12-19 and the susceptible line 91-112. The expression of BrWAK1 could be induced by salicylic acid and pathogen inoculation. Expression of BrWAK1 in 91-112 could significantly enhance resistance to the pathogen, while truncating BrWAK1 in T12-19 increased disease susceptibility. Variation in the extracellular galacturonan binding (GUB) domain of BrWAK1 was found to mainly confer resistance to downy mildew in T12-19. Moreover, BrWAK1 was proved to interact with BrBAK1 (brassinosteroid insensitive 1 associated kinase), resulting in the activation of the downstream mitogen-activated protein kinase (MAPK) cascade to trigger the defence response. BrWAK1 is the first identified and thoroughly characterized WAK gene conferring disease resistance in Chinese cabbage, and the plant biomass is not significantly influenced by BrWAK1, which will greatly accelerate Chinese cabbage breeding for downy mildew resistance.

The Responses of a Grapevine Rhizosphere System to Mulching Using Amplicon Sequencing and Transcriptomic Analysis

Although mulching is a widely used agronomic practice, its effects on the rhizosphere remain poorly understood. Here, we employed amplicon and transcriptomic sequencing to investigate variations in a grapevine rhizosphere system under mulch treatment (rice straw + felt + plastic film). Analyzing 16S and intergenic spacer (ITS) rRNA sequences indicated that the Shannon and Simpson indices of the bacterial and fungal communities increased markedly under mulch treatment. The bacterial and fungal compositions varied significantly between the control and mulch treatments. Mulching enriched for potentially beneficial microbes that confer disease resistance to plants or participate in nitrogen metabolism (Kaistobacter, Ammoniphilus, Lysobacter, Ammoniphilus, Alicyclobacillus, Aquicella, Nitrospira, Chaetomium, and Microascus), whereas more potentially pathogenic microbes (Fusarium and Gibberella) were detected in the control. Moreover, certain bacteria and fungi exhibited different correlations with the root transcriptome functions of the MEBlue module. The complexity of the bacterial and fungal co-occurrence networks increased with higher node numbers, positive and negative links after mulching. Following mulching, the rhizosphere showed elevated pH, organic matter, and catalase activities, and decreased sucrase and cellulase and β-glucosidase activities. Our results provide comprehensive data showing how a grapevine rhizosphere system responded to mulching treatment and shed important insight into mulching practices for fruit trees.

Dynamics of reactive oxygen species and lignin biosynthesis during leaf spot disease of Withania somnifera (L.) Dunal.

Withania somnifera is an important medicinal plant, however, its cultivation and quality are compromised through infestation by leaf spot disease caused by the fungus, Alternaria alternata. To find suitable strategies against this disease, studies on post-infectional changes are important. ROS are critical as they interact with other defence signalling pathways. We analyzed ROS-generating and scavenging systems in healthy and diseased leaf samples of W. somnifera and ROS-driven downstream defence pathways. We used DAB and NBT assays for ROS detection, spectrophotometry and in-gel assays for ROS scavenging enzymes, a thioglycolic acid (TGA) based assay, histochemical staining for lignin, and qRT-PCR for transcript-level expression. Leaf spot infection in W. somnifera increased NADPH oxidase activity and ROS accumulation in infected leaves, together with enhanced antioxidant enzyme activity. Leaf spot-infected leaves had increased lignin content and higher expression of lignin biosynthesis genes. In addition, transcript levels of defence-related genes, NPR1 and PR, were also upregulated. The present work provides insights into responses to leaf spot disease through defence-related signalling in W. somnifera. It demonstrates crosstalk between ROS and lignin biosynthesis. This work identified potential targets for developing strategies to confer disease resistance against A. alternata in W. somnifera.

The self-association of cytoplasmic malate dehydrogenase 1 promotes malate biosynthesis and confers disease resistance in cassava

Malate dehydrogenase (MDH) as an essential metabolic enzyme is widely involved in plant developmental processes. However, the direct relationship between its structural basis and in vivo roles especially in plant immunity remains elusive. In this study, we found that cytoplasmic cassava (Manihot esculenta, Me) MDH1 was essential for plant disease resistance against cassava bacterial blight (CBB). Further investigation revealed that MeMDH1 positively modulated cassava disease resistance, accompanying the regulation of salicylic acid (SA) accumulation and pathogensis-related protein 1 (MePR1) expression. Notably, the metabolic product of MeMDH1 (malate) also improved disease resistance in cassava, and its application rescued the disease susceptibility and decreased immune responses of MeMDH1-silenced plants, indicating that malate was responsible for MeMDH1-mediated disease resistance. Interestingly, MeMDH1 relied on Cys330 residues to form homodimer, which was directly related with MeMDH1 enzyme activity and the corresponding malate biosynthesis. The crucial role of Cys330 residue in MeMDH1 was further confirmed by in vivo functional comparison between overexpression of MeMDH1 and MeMDH1C330A in cassava disease resistance. Taken together, this study highlights that MeMDH1 confers improved plant disease resistance through protein self-association to promote malate biosynthesis, extending the knowledge of the relationship between its structure and cassava disease resistance.

Transcriptome-Assisted SNP Marker Discovery for Phytophthora infestans Resistance in Solanum lycopersicum L.

Late blight, caused by oomycetes Phytophthora infestans is one of the most challenging fungal diseases to manage in tomato plants (Solanum lycopersicum L.). Toward managing the disease, conventional breeding has successfully introgressed genetic loci conferring disease resistance from various wild relatives of tomato into commercial varieties. The cataloging of disease-associated SNP markers and a deeper understanding of disease-resistance mechanisms are needed to keep up with the demand for commercial varieties resistant against emerging pathogen strains. To this end, we performed transcriptome sequencing to evaluate the gene expression dynamics of tomato varieties, resistant and susceptible to Phytophthora infection. Further integrating the transcriptome dataset with large-scale public genomic data of varieties with known disease phenotypes, a panel of single nucleotide polymorphism (SNP) markers correlated with disease resistance was identified. These SNPs were then validated on 31 lines with contrasting phenotypes for late blight. The identified SNPs are located on genes coding for a putative cysteine-rich transmembrane module (CYSTM), Solyc09g098310, and a nucleotide-binding site-leucine-rich repeat protein, Solyc09g098100, close to the well-studied Ph-3 resistance locus known to have a role in plant immunity against fungal infections. The panel of SNPs generated by this study using transcriptome sequencing showing correlation with disease resistance across a broad set of plant material can be used as markers for molecular screening in tomato breeding.

Maternal diet modulates the infant microbiome and intestinal Flt3L necessary for dendritic cell development and immunity to respiratory infection

Poor maternal diet during pregnancy is a risk factor for severe lower respiratory infections (sLRIs) in the offspring, but the underlying mechanisms remain elusive. Here, we demonstrate that in mice a maternal low-fiber diet (LFD) led to enhanced LRI severity in infants because of delayed plasmacytoid dendritic cell (pDC) recruitment and perturbation of regulatory Tcell expansion in the lungs. LFD altered the composition of the maternal milk microbiome and assembling infant gut microbiome. These microbial changes reduced the secretion of the DC growth factor Flt3L by neonatal intestinal epithelial cells and impaired downstream pDC hematopoiesis. Therapy with a propionate-producing bacteria isolated from the milk of high-fiber diet-fed mothers, or supplementation with propionate, conferred protection against sLRI by restoring gut Flt3L expression and pDC hematopoiesis. Our findings identify a microbiome-dependent Flt3L axis in the gut that promotes pDC hematopoiesis in early life and confers disease resistance against sLRIs.

Nucleotide-binding leucine-rich repeat network underlies nonhost resistance of pepper against the Irish potato famine pathogen Phytophthora infestans.

Nonhost resistance (NHR) is a robust plant immune response against non-adapted pathogens. A number of nucleotide-binding leucine-rich repeat (NLR) proteins that recognize non-adapted pathogens have been identified, although the underlying molecular mechanisms driving robustness of NHR are still unknown. Here, we screened 57 effectors of the potato late blight pathogen Phytophthora infestans in nonhost pepper (Capsicum annuum) to identify avirulence effector candidates. Selected effectors were tested against 436 genome-wide cloned pepper NLRs, and we identified multiple functional NLRs that recognize P. infestans effectors and confer disease resistance in the Nicotiana benthamiana as a surrogate system. The identified NLRs were homologous to known NLRs derived from wild potatoes that recognize P. infestans effectors such as Avr2, Avrblb1, Avrblb2, and Avrvnt1. The identified CaRpi-blb2 is a homologue of Rpi-blb2, recognizes Avrblb2 family effectors, exhibits feature of lineage-specifically evolved gene in microsynteny and phylogenetic analyses, and requires pepper-specific NRC (NLR required for cell death)-type helper NLR for proper function. Moreover, CaRpi-blb2-mediated hypersensitive response and blight resistance were more tolerant to suppression by the PITG_15 278 than those mediated by Rpi-blb2. Combined results indicate that pepper has stacked multiple NLRs recognizing effectors of non-adapted P. infestans, and these NLRs could be more tolerant to pathogen-mediated immune suppression than NLRs derived from the host plants. Our study suggests that NLRs derived from nonhost plants have potential as untapped resources to develop crops with durable resistance against fast-evolving pathogens by stacking the network of nonhost NLRs into susceptible host plants.

Plant Protection against Viruses: An Integrated Review of Plant Immunity Agents.

Plant viruses are an important class of pathogens that seriously affect plant growth and harm crop production. Viruses are simple in structure but complex in mutation and have thus always posed a continuous threat to agricultural development. Low resistance and eco-friendliness are important features of green pesticides. Plant immunity agents can enhance the resilience of the immune system by activating plants to regulate their metabolism. Therefore, plant immune agents are of great importance in pesticide science. In this paper, we review plant immunity agents, such as ningnanmycin, vanisulfane, dufulin, cytosinpeptidemycin, and oligosaccharins, and their antiviral molecular mechanisms and discuss the antiviral applications and development of plant immunity agents. Plant immunity agents can trigger defense responses and confer disease resistance to plants, and the development trends and application prospects of plant immunity agents in plant protection are analyzed in depth.

Novel EIicitin from Pythium oligandrum Confers Disease Resistance against Phytophthora capsici in Solanaceae Plants.

The mycoparasite Pythium oligandrum is a nonpathogenic oomycete that can boost plant immune responses. Elicitins are microbe-associated molecular patterns (MAMPs) specifically produced by oomycetes that activate plant defense. Here, we identified a novel elicitin, PoEli8, from P. oligandrum that exhibits immunity-inducing activity in plants. In vitro-purified PoEli8 induced strong innate immune responses and enhanced resistance to the oomycete pathogen Phytophthora capsici in Solanaceae plants, including Nicotiana benthamiana, tomato, and pepper. Cell death and reactive oxygen species (ROS) accumulation triggered by the PoEli8 protein were dependent on the plant coreceptors receptor-like kinases (RLKs) BAK1 and SOBIR1. Furthermore, REli from N. benthamiana, a cell surface receptor-like protein (RLP) was implicated in the perception of PoEli8 in N. benthamiana. These results indicate the potential value of PoEli8 as a bioactive formula to protect Solanaceae plants against Phytophthora.