Capsici Infection Research Articles

A Genome-Wide Analysis of Pathogenesis-Related Protein-1 (PR-1) Genes from Piper nigrum Reveals Its Critical Role during Phytophthora capsici Infection.

Black pepper (Piper nigrum L.) is a prominent spice that is an indispensable ingredient in cuisine and traditional medicine. Phytophthora capsici, the causative agent of footrot disease, causes a drastic constraint in P. nigrum cultivation and productivity. To counterattack various biotic and abiotic stresses, plants employ a broad array of mechanisms that includes the accumulation of pathogenesis-related (PR) proteins. Through a genome-wide survey, eleven PR-1 genes that belong to a CAP superfamily protein with a caveolin-binding motif (CBM) and a CAP-derived peptide (CAPE) were identified from P. nigrum. Despite the critical functional domains, PnPR-1 homologs differ in their signal peptide motifs and core amino acid composition in the functional protein domains. The conserved motifs of PnPR-1 proteins were identified using MEME. Most of the PnPR-1 proteins were basic in nature. Secondary and 3D structure analyses of the PnPR-1 proteins were also predicted, which may be linked to a functional role in P. nigrum. The GO and KEGG functional annotations predicted their function in the defense responses of plant-pathogen interactions. Furthermore, a transcriptome-assisted FPKM analysis revealed PnPR-1 genes mapped to the P. nigrum-P. capsici interaction pathway. An altered expression pattern was detected for PnPR-1 transcripts among which a significant upregulation was noted for basic PnPR-1 genes such as CL10113.C1 and Unigene17664. The drastic variation in the transcript levels of CL10113.C1 was further validated through qRT-PCR and it showed a significant upregulation in infected leaf samples compared with the control. A subsequent analysis revealed the structural details, phylogenetic relationships, conserved sequence motifs and critical cis-regulatory elements of PnPR-1 genes. This is the first genome-wide study that identified the role of PR-1 genes during P. nigrum-P. capsici interactions. The detailed in silico experimental analysis revealed the vital role of PnPR-1 genes in regulating the first layer of defense towards a P. capsici infection in Panniyur-1 plants.

The dissection of R genes and locus Pc5.1 in Phytophthora capsici infection provides a novel view of disease resistance in peppers

BackgroundPhytophthora capsici root rot (PRR) is a disastrous disease in peppers (Capsicum spp.) caused by soilborne oomycete with typical symptoms of necrosis and constriction at the basal stem and consequent plant wilting. Most studies on the QTL mapping of P. capsici resistance suggested a consensus broad-spectrum QTL on chromosome 5 named Pc.5.1 regardless of P. capsici isolates and resistant resources. In addition, all these reports proposed NBS-ARC domain genes as candidate genes controlling resistance.ResultsWe screened out 10 PRR-resistant resources from 160 Capsicum germplasm and inspected the response of locus Pc.5.1 and NBS-ARC genes during P. capsici infection by comparing the root transcriptomes of resistant pepper 305R and susceptible pepper 372S. To dissect the structure of Pc.5.1, we anchored genetic markers onto pepper genomic sequence and made an extended Pc5.1 (Ext-Pc5.1) located at 8.35 Mb–38.13 Mb on chromosome 5 which covered all Pc5.1 reported in publications. A total of 571 NBS-ARC genes were mined from the genome of pepper CM334 and 34 genes were significantly affected by P. capsici infection in either 305R or 372S. Only 5 inducible NBS-ARC genes had LRR domains and none of them was positioned at Ext-Pc5.1. Ext-Pc5.1 did show strong response to P. capsici infection and there were a total of 44 differentially expressed genes (DEGs), but no candidate genes proposed by previous publications was included. Snakin-1 (SN1), a well-known antimicrobial peptide gene located at Pc5.1, was significantly decreased in 372S but not in 305R. Moreover, there was an impressive upregulation of sugar pathway genes in 305R, which was confirmed by metabolite analysis of roots. The biological processes of histone methylation, histone phosphorylation, DNA methylation, and nucleosome assembly were strongly activated in 305R but not in 372S, indicating an epigenetic-related defense mechanism.ConclusionsThose NBS-ARC genes that were suggested to contribute to Pc5.1 in previous publications did not show any significant response in P. capsici infection and there were no significant differences of these genes in transcription levels between 305R and 372S. Other pathogen defense-related genes like SN1 might account for Pc5.1. Our study also proposed the important role of sugar and epigenetic regulation in the defense against P. capsici.

Antimicrobial mechanisms of g-C3N4 nanosheets against the oomycetes Phytophthora capsici: Disrupting metabolism and membrane structures and inhibiting vegetative and reproductive growth

To understand the potential of urea-synthesized g-C3N4 nanosheets (0.125–1 mg/mL) as antimicrobial agents against oomycetes, an investigation of the interaction mechanism between g-C3N4 nanosheets and Phytophthora capsici was conducted. Transcription analysis showed that after being exposed to g-C3N4 nanosheets for 1 h, P. capsici triggered a sharp upregulation of antioxidant activities and structural constituents and a downregulation of metabolic pathways, including ATP generation, autophagy disruption, membrane system disorders and other complex adaptive processes. All the life stages of P. capsici, including mycelial growth, sporangium formation, zoospore numbers and zoospore germination were remarkably inhibited and even injured. A mutual mechanism is proposed in this work: ROS stress upon exposure to visible irradiation and, combined with their sharp nanosheet structure, cause perturbations of the cell membrane and induce damage to the ultrastructure of mycelial growth, sporangium and zoospores. Given that the antimicrobial action of g-C3N4 nanosheets were derived from the damage throughout the duration of treatment and was not limited to a single target, these complex mechanisms could favor the avoidance of drug resistance and benefit other oomycetes management. More importantly, in addition to restraining P. capsici infection in host plants, g-C3N4 nanosheets promoted pepper plant growth. Hence, g-C3N4 nanosheets have potential as a new non-metal antimicrobial agent to control oomycotal disease in crops.

A Phytophthora sojae CRN effector mediates phosphorylation and degradation of plant aquaporin proteins to suppress host immune signaling.

Phytophthora genomes encode a myriad of Crinkler (CRN) effectors, some of which contain putative kinase domains. Little is known about the host targets of these kinase-domain-containing CRNs and their infection-promoting mechanisms. Here, we report the host target and functional mechanism of a conserved kinase CRN effector named CRN78 in a notorious oomycete pathogen, Phytophthora sojae. CRN78 promotes Phytophthora capsici infection in Nicotiana benthamiana and enhances P. sojae virulence on the host plant Glycine max by inhibiting plant H2O2 accumulation and immunity-related gene expression. Further investigation reveals that CRN78 interacts with PIP2-family aquaporin proteins including NbPIP2;2 from N. benthamiana and GmPIP2-13 from soybean on the plant plasma membrane, and membrane localization is necessary for virulence of CRN78. Next, CRN78 promotes phosphorylation of NbPIP2;2 or GmPIP2-13 using its kinase domain in vivo, leading to their subsequent protein degradation in a 26S-dependent pathway. Our data also demonstrates that NbPIP2;2 acts as a H2O2 transporter to positively regulate plant immunity and reactive oxygen species (ROS) accumulation. Phylogenetic analysis suggests that the phosphorylation sites of PIP2 proteins and the kinase domains of CRN78 homologs are highly conserved among higher plants and oomycete pathogens, respectively. Therefore, this study elucidates a conserved and novel pathway used by effector proteins to inhibit host cellular defenses by targeting and hijacking phosphorylation of plant aquaporin proteins.

SORF-Encoded Polypeptide SEP1 Is a Novel Virulence Factor of Phytophthora Pathogens.

Diseases caused by the notorious Phytophthora spp. result in enormous economic losses to crops and forests. Increasing evidence suggests that small open reading frame-encoded polypeptides (SEPs) participate in environmental responses of animals, plants, and fungi. However, it remains largely unknown whether Phytophthora pathogens produce SEPs. Here, we systematically predicted and identified 96 SEP candidates in P. capsici. Among them, three may induce stable cell death in Nicotiana benthamiana. Phytophthora-specific and conserved SEP1 facilitated P. capsici infection. PcSEP1-induced cell death is BAK1 and SOBIR1 independent and is correlated with its virulence function. Finally, PcSEP1 may be targeted to the apoplast for carrying out its functions, for which the C terminus is indispensable. Together, our results demonstrated that SEP1 is a new virulence factor, and previously unknown SEPs may act as effector proteins in Phytophthora pathogens.[Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

To evaluate in vitro the efficacy of fungicides, bio-control agents and plant extract against Colletotrichum capsici

Colletotrichum capsici infection will be higher in the mature stage of chilli plant than in the early stage of plant (Krairuan et al., 2008). The fungus prefers warm humid environment for spreading the anthracnose disease uniformly and effectively. All the two contact and six systemic fungicides evaluated in vitro were found fungistatic against Colletotrichum capsici. Among all these fungicides, Tricyclazole was found to be most effective with significantly maximum mycelial growth inhibition and least mycelial growth followed by fungicides viz. Azostrobin, Tebuconazole, Difenconazole, Propiconazole, Carbendazim + Mancozeb. While comparatively minimum average radial mycelial growth inhibition was recorded with Hexaconazole followed by Propineb. All the seven fungal and one bacterial antagonists evaluated in vitro were found antifungal against Colletotrichum capsici exhibited significant mycelial growth inhibition. However, Trichoderma asperallum, Pseudomonas fluorescens, Trichoderma harzianum and Gliocladium virens recorded significantly highest mycelial growth inhibition. Rest of the bioagents, Trichoderma ligronum, Trichoderma koningii and Trichoderma longibrachiatum and Trichoderma hamatum tested also caused significant mycelial inhibition of the test pathogen.

A Diagnostic Guide for Phytophthora capsici Infecting Vegetable Crops

Phytophthora capsici is an oomycete pathogen causing economically important diseases in a wide range of hosts worldwide including cucurbitaceous, solanaceous, and fabaceous crops. All plant parts, crown and roots, or only the fruit may be affected depending on the host, and symptoms can range from wilting to rot and plant death. Considered a hemibiotroph, P. capsici can be cultured in artificial media and maintained in long-term storage. In this diagnostic guide, we describe methods to identify P. capsici infection based on disease symptoms and pathogen signs. We also outline methods for molecular identification, pathogen isolation, storage of single-sporangium cultures, and pathogenicity testing.

Plasmopara viticola effector PvRXLR111 stabilizes VvWRKY40 to promote virulence.

Plasmopara viticola, the causal organism of grapevine downy mildew, secretes a vast array of effectors to manipulate host immunity. Previously, several cell death‐inducing PvRXLR effectors have been identified, but their functions and host targets are poorly understood. Here, we investigated the role of PvRXLR111, a cell death‐inducing RXLR effector, in manipulating plant immunity. When coexpressed with other PvRXLR effectors, PvRXLR111‐induced cell death was prevented. Transient expression of PvRXLR111 in Nicotiana benthamiana suppressed bacterial flagellin peptide flg22‐elicited immune responses and enhanced Phytophthora capsici infection. PvRXLR111 induction in Arabidopsis increased susceptibility to Hyaloperonospora arabidopsidis. PvRXLR111 expression in Pseudomonas syringae promoted bacterial colonization. By immunoprecipitation‐mass spectrometry analysis, yeast two‐hybrid, pull‐down, and bimolecular fluorescence complementation assays, it was shown that PvRXLR111 interacted with Vitis vinifera putative WRKY transcription factor 40 (VvWRKY40), which increased VvWRKY40 stability. Transient expression of VvWRKY40 in N. benthamiana inhibited flg22‐induced reactive oxygen species burst and enhanced P. capsici infection and silencing NbWRKY40 attenuated P. capsici colonization. These results suggest VvWRKY40 functions as a negative regulator in plant immunity and that PvRXLR111 suppresses host immunity by stabilizing VvWRKY40.

CaSBP11 Participates in the Defense Response of Pepper to Phytophthora capsici through Regulating the Expression of Defense-Related Genes.

Squamosa promoter binding protein (SBP)-box genes are plant-specific transcription factors involved in plant growth and development, morphogenesis and biotic and abiotic stress responses. However, these genes have been understudied in pepper, especially with respect to defense responses to Phytophthora capsici infection. CaSBP11 is a SBP-box family gene in pepper that was identified in our previous research. Silencing CaSBP11 enhanced the defense response of pepper plants to Phytophthora capsici. Without treatment, the expression of defense-related genes (CaBPR1, CaPO1, CaSAR8.2 and CaDEF1) increased in CaSBP11-silenced plants. However, the expression levels of these genes were inhibited under transient CaSBP11 expression. CaSBP11 overexpression in transgenic Nicotiana benthamiana decreased defense responses, while in Arabidopsis, it induced or inhibited the expression of genes in the salicylic acid and jasmonic acid signaling pathways. CaSBP11 overexpression in sid2-2 mutants induced AtNPR1, AtNPR3, AtNPR4, AtPAD4, AtEDS1, AtEDS5, AtMPK4 and AtNDR1 expression, while AtSARD1 and AtTGA6 expression was inhibited. CaSBP11 overexpression in coi1-21 and coi1-22 mutants, respectively, inhibited AtPDF1.2 expression and induced AtPR1 expression. These results indicate CaSBP11 has a negative regulatory effect on defense responses to Phytophthora capsici. Moreover, it may participate in the defense response of pepper to Phytophthora capsici by regulating defense-related genes and the salicylic and jasmonic acid-mediated disease resistance signaling pathways.

Concurrent Metabolic Profiling and Quantification of Aromatic Amino Acids and Phytohormones in Solanum lycopersicum Plants Responding to Phytophthora capsici.

Pathogenic microorganisms account for large production losses in the agricultural sector. Phytophthora capsici is an oomycete that causes blight and fruit rot in important crops, especially those in the Solanaceae family. P. capsici infection is difficult to control due to genetic diversity, arising from sexual reproduction, and resistant spores that remain dormant in soil. In this study, the metabolomics of tomato plants responding to infection by P. capsici were investigated. Non-targeted metabolomics, based on liquid chromatography coupled to mass spectrometry (LC-MS), were used with multivariate data analyses to investigate time-dependent metabolic reprogramming in the roots, stems, and leaves of stem-infected plants, over an 8 day period. In addition, phytohormones and amino acids were determined using quantitative LC-MS. Methyl salicylate and 1-aminocyclopropane-1-carboxylate were detected as major signalling molecules in the defensive response to P. capsici. As aromatic amino acid precursors of secondary metabolic pathways, both phenylalanine and tryptophan showed a continuous increase over time in all tissues, whereas tyrosine peaked at day 4. Non-targeted metabolomic analysis revealed phenylpropanoids, benzoic acids, glycoalkaloids, flavonoids, amino acids, organic acids, and fatty acids as the major classes of reprogrammed metabolites. Correlation analysis showed that metabolites derived from the same pathway, or synthesised by different pathways, could either have a positive or negative correlation. Furthermore, roots, stems, and leaves showed contrasting time-dependent metabolic reprogramming, possibly related to the biotrophic vs. necrotrophic life-stages of the pathogen, and overlapping biotic and abiotic stress signaling. As such, the targeted and untargeted approaches complemented each other, to provide a detailed view of key time-dependent metabolic changes, occurring in both the asymptomatic and symptomatic stages of infection.

Endophytic bacteria from Piper colubrinum suppress Phytophthora capsici infection in black pepper (Piper nigrum L.) and improve plant growth in the nursery

Foot rot caused by Phytophthora capsici is a threat for black pepper cultivation. No cultivated variety is resistant to the disease. Endophytic bacteria were obtained from the roots, stem and leaves of Piper colubrinum, a wild relative of black pepper, resistant to P. capsici. In vitro dual culture plate assay showed that seven among them were antagonistic against P. capsici. Lesion suppression assay on detached black pepper leaves showed that leaves treated with the isolate Bacillus velezensis PCSE10 caused 79.02% disease suppression. In greenhouse experiment the lowest disease index occurred in plants treated with Rhizobium radiobacter PCRE10 with 75.05% disease suppression. The endophytes improved growth of black pepper in the nursery when the cuttings were bacterized and planted. We report for the first time that the wild relative of black pepper, P. colubrinum is a good source of antagonistic bacteria against P. capsici causing foot rot disease of black pepper.

Phenotypic characterization of chili pepper (Capsicum annuum L.) under Phytophthora capsici infection and analysis of genetic diversity among identified resistance accessions using SSR markers

Chili pepper (Capsicum annuum L.) is one of the most important vegetable crops, largely suffers from various biotic stresses, including Phytophthora capsici L., imposing huge yield loss. Due to the lack of agronomically superior traits in available resistant accessions, chili breeders are constantly searching for new sources of resistance with genetically diverse traits. In the present study, a total of 233 chili pepper accessions from Ethiopia and India were screened under P. capsici infection. A total of 22 highly resistant and 17 moderately resistant accessions were identified. Among these, only 32 chili pepper accessions with mean disease index ranging from 1.4 to 2.0 and 2.20–3.8, were selected for genetic diversity analysis. From a total of 19 SSR primers analyzed, only 14 SSR primers were shown to be polymorphic. The result showed that a total of 31 alleles with an average of 2.214 alleles per primer were amplified across the selected accessions. A maximum of 3 alleles were observed in only 3 SSR primers. The analysis of 14 SSR primers resulted in PIC values ranging from 0.12 to 0.98 with an average of 0.64, the percentage of polymorphic loci of 11.45–96.87% with an average of 57.69% and effective number of alleles (Ne) of 1.058–2.174 with a mean of 2.213. This indicated that the 14 SSR primers detected variation among 32 chili pepper accessions. The genetic dissimilarity index (GDI) value ranged from 0.05 to 0.51, with the highest GDI (0.51) in Gutowayu_80039 and IC_537646 accessions. The population structure and cluster analysis grouped the chili pepper accessions into three genetic resistance groups. In addition, the UPGMA cluster analysis of the 14 SSR primers clearly distinguished between one resistance group and the other. As per AMOVA analysis, a total of 42% and 58% of variation among and within populations were detected in the nine populations of C. annuum, respectively. The resistance/moderate resistance accessions greatly showed both phenotypic and genotypic variation. The accessions GojamMecha_9082, Mareko_233636, GojamMecha_9086, IC_526851, and IC_537587 showed high level of resistance with diversified resistance loci, which could be used as a source of resistance for chili pepper breeders.

High-Throughput Sequencing-Based Identification of Arabidopsis miRNAs Induced by Phytophthora capsici Infection.

MicroRNAs (miRNAs) are a group of small non-coding endogenous RNAs. In plants, miRNAs play vital functions in regulating growth, development, and stress response. However, the role of miRNAs in Arabidopsis-Phytophthora capsici (P. capsici) model pathosystem is poorly understood. Here, we used a high-throughput sequencing approach to identify pathogen-responsive miRNAs using 15 small RNA (sRNA) libraries prepared from Arabidopsis thaliana leaves collected at 0, 3, 6, 12, and 24 h post-inoculation with P. capsici. A total of 293 known miRNAs and 6 potential novel sRNAs (miRNAs or siRNAs) were identified, of which 33 miRNAs were differentially expressed at four different infection stages. To verify the reliability of the sRNA-seq results, we investigated the expression of five sRNAs upregulated throughout the four infection stages and their potential target genes using northern blot analysis and/or stem-loop quantitative real-time polymerase chain reaction (qRT-PCR). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses revealed that the potential target genes of the differentially expressed miRNAs, both conserved and novel, were enriched in pathways such as starch and sugar metabolism, spliceosome, and plant-pathogen interaction, indicating that the splicing machinery and pathogenesis-related (PR) proteins play important roles in the response to P. capsici infection. Taken together, these results provide novel insights into the molecular mechanisms of pathogenesis by P. capsici. Additionally, these results will serve as a strong foundation for further in-depth analysis of miRNAs involved in the resistance to Phytophthora species in other crops.

The transcriptional reprograming and functional identification of WRKY family members in pepper\u2019s response to Phytophthora capsici infection

BackgroundPlant transcription factors (TFs) are key transcriptional regulators to manipulate the regulatory network of host immunity. However, the globally transcriptional reprogramming of plant TF families in response to pathogens, especially between the resistant and susceptible host plants, remains largely unknown.ResultsHere, we performed time-series RNA-seq from a resistant pepper line CM334 and a susceptible pepper line EC01 upon challenged with Phytophthora capsici, and enrichment analysis indicated that WRKY family most significantly enriched in both CM334 and EC01. Interestingly, we found that nearly half of the WRKY family members were significantly up-regulated, whereas none of them were down-regulated in the two lines. These induced WRKY genes were greatly overlapped between CM334 and EC01. More strikingly, most of these induced WRKY genes were expressed in time-order patterns, and could be mainly divided into three subgroups: early response (3 h-up), mid response (24 h-up) and mid-late response (ML-up) genes. Moreover, it was found that the responses of these ML-up genes were several hours delayed in EC01. Furthermore, a total of 19 induced WRKY genes were selected for functional identification by virus-induced gene silencing. The result revealed that silencing of CaWRKY03–6, CaWRKY03–7, CaWRKY06–5 or CaWRKY10–4 significantly increase the susceptibility to P. capsici both in CM334 and EC01, indicating that they might contribute to pepper’s basal defense against P. capsici; while silencing of CaWRKY08–4 and CaWRKY01–10 significantly impaired the disease resistance in CM334 but not in EC01, suggesting that these two WRKY genes are prominent modulators specifically in the resistant pepper plants.ConclusionsThese results considerably extend our understanding of WRKY gene family in pepper’s resistance against P. capsici and provide potential applications for genetic improvement against phytophthora blight.

Identification of Pepper CaSBP08 Gene in Defense Response Against Phytophthora capsici Infection.

Little information is available on the role of Squamosa promoter binding protein (SBP)-box genes in pepper plants. This family of genes is known to have transcription characteristics specific to plants and to regulate plant growth, development, stress responses, and signal transduction. To investigate their specific effects in pepper (Capsicum annuum), we screened pepper SBP-box family genes (CaSBP genes) for Phytophthora capsici (P. capsici) resistance genes using virus-induced gene silencing. CaSBP08, CaSBP11, CaSBP12, and CaSBP13, which are associated with plant defense responses against P. capsici, were obtained from among fifteen identified CaSBP genes. The function of CaSBP08 was identified in pepper defense response against P. capsici infection in particular. CaSBP08 protein was localized to the nucleus. Silencing of CaSBP08 enhanced resistance to P. capsici infection. Following P. capsici inoculation, the malondialdehyde content, peroxidase activity, and disease index percentage of the CaSBP08-silenced plants decreased compared to the control. Additionally, the expression levels of other defense-related genes, especially those of CaBPR1 and CaSAR8.2, were more strongly induced in CaSBP08-silenced plants than in the control. However, CaSBP08 overexpression in Nicotiana benthamiana enhanced susceptibility to P. capsici infection. This work provides a foundation for the further research on the role of CaSBP genes in plant defense responses against P. capsici infection.

The CaChiVI2 Gene of Capsicum annuum L. Confers Resistance Against Heat Stress and Infection of Phytophthora capsici.

Extreme environmental conditions seriously affect crop growth and development, resulting in substantial reduction in yield and quality. However, chitin-binding proteins (CBP) family member CaChiVI2 plays a crucial role in eliminating the impact of adverse environmental conditions, such as cold and salt stress. Here, for the first time it was discovered that CaChiVI2 (Capana08g001237) gene of pepper (Capsicum annuum L.) had a role in resistance to heat stress and physiological processes. The full-length open-reading frame (ORF) of CaChiVI2 (606-bp, encoding 201-amino acids), was cloned into TRV2:CaChiVI2 vector for silencing. The CaChiVI2 gene carries heat shock elements (HSE, AAAAAATTTC) in the upstream region, and thereby shows sensitivity to heat stress at the transcriptional level. The silencing effect of CaChiVI2 in pepper resulted in increased susceptibility to heat and Phytophthora capsici infection. This was evident from the severe symptoms on leaves, the increase in superoxide (O2–) and hydrogen peroxide (H2O2) accumulation, higher malondialdehyde (MDA), relative electrolyte leakage (REL) and lower proline contents compared with control plants. Furthermore, the transcript level of other resistance responsive genes was also altered. In addition, the CaChiIV2-overexpression in Arabidopsis thaliana showed mild heat and drought stress symptoms and increased transcript level of a defense-related gene (AtHSA32), indicating its role in the co-regulation network of the plant. The CaChiVI2-overexpressed plants also showed a decrease in MDA contents and an increase in antioxidant enzyme activity and proline accumulation. In conclusion, the results suggest that CaChiVI2 gene plays a decisive role in heat and drought stress tolerance, as well as, provides resistance against P. capsici by reducing the accumulation of reactive oxygen species (ROS) and modulating the expression of defense-related genes. The outcomes obtained here suggest that further studies should be conducted on plants adaptation mechanisms in variable environments.

Transcriptome analysis clarified genes involved in resistance to Phytophthora capsici in melon.

Phytophthora blight caused by Phytophthora capsici is a devastating disease for melon plant. However, the underlying resistance mechanisms are still poorly understood. In this study, the transcriptome differences between the resistant ZQK9 and susceptible E31 at 0, 3, and 5 days post-inoculation (dpi) were identified by RNA-seq. A total of 1,195 and 6,595 differentially expressed genes (DEGs) were identified in ZQK9 and E31, respectively. P. capsici infection triggered massive transcript changes in the inoculated tissues. Genes related to plant defense responses were activated, which was reflected by a lot of up-regulated DEGs involved in pathogenesis-related (PR) genes, hormones biosynthesis and signal transduction, secondary metabolites biosynthesis and cell wall modification in resistant ZQK9. The dataset generated in this study may provide a basis for identifying candidate resistant genes in melon against P. capsici and lay a foundation for further research on the molecular mechanisms.

Acibenzolar-S-methyl and β-amino butyric acid-induced upregulation of biochemical defense against Colletotrichum capsici infection in chilli (Capsicum annuum)

Abiotic inducers (AI) are synthetic/natural compound, induces systemic resistance in plants against pathogens. Present study aimed to evaluate the foliar application of AI [Acibenzolar-S-Methyl (ASM), and β-Amino Butyric Acid (BABA)] in managing chilli anthracnose under greenhouse conditions. Foliar applications of ASM-5 μg/ml and BABA-10 mM significantly decreases disease incidence to 13.15% and 14.1% respectively, when compared to respective controls (65% and 65.34%). AI treated seedlings recorded maximum H2O2 accumulation at 9 h (ASM) and 12 h (BABA) after challenged with pathogen. In AI treated seedlings, activity of defense-related enzymes (Phenylalanine ammonia-lyase, Peroxidase, Polyphenol oxidase, Lipoxygenase, and chitinase) was upregulated after challenge inoculation. Similarly, maximum phenolic (μg gallic acid/g tissue) accumulation of 147 and 71.2 was recorded with ASM and BABA treatment, respectively. The AI induced changes in biochemical parameters are in correlation with reduced disease incidence. Hence, AI can use as alternative, safe and eco-friendly candidate to manage chilli anthracnose.

A Phytophthora capsici effector suppresses plant immunity via interaction with EDS1.

EDS1 (Enhanced Disease Susceptibility 1) plays a crucial role in both effector‐triggered immunity activation and plant basal defence. However, whether pathogen effectors can target EDS1 or an EDS1‐related pathway to manipulate immunity is rarely reported. In this study, we identified a Phytophthora capsici Avirulence Homolog (Avh) RxLR (Arg‐any amino acid‐Leu‐Arg) effector PcAvh103 that interacts with EDS1. We demonstrated that PcAvh103 can facilitate P. capsici infection and is required for pathogen virulence. Furthermore, genetic evidence showed that PcAvh103 contributes to virulence through targeting EDS1. Finally, PcAvh103 specifically interacts with the lipase domain of EDS1 and can promote the disassociation of EDS1–PAD4 (Phytoalexin Deficient 4) complex in planta. Together, our results revealed that the P. capsici RxLR effector PcAvh103 targets host EDS1 to suppress plant immunity, probably through disrupting the EDS1–PAD4 immune signalling pathway.

Two phosphatidylinositol 3-kinase components are involved in interactions between Nicotiana benthamiana and Phytophthora by regulating pathogen effectors and host cell death.

Phosphatidylinositol 3-phosphate (PtdIns(3)P) has been reported to regulate different physiological processes in plants. PtdIns(3)P is synthesised by the phosphatidylinositol 3-kinase (PI3K) complex which includes common subunits of vacuolar protein sorting (VPS)15, VPS30 and VPS34. Here, we characterised the roles of the important genes NbVPS15, -30 and -34 encoding PI3K components during interactions between Nicotiana benthamiana and Phytophthora pathogens. NbVPS15 and NbVPS34 were upregulated during infection, and plants deficient in these two genes displayed higher resistance to two different Phytophthora pathogens. Silencing NbVPS15 and NbVPS34 decreased the content of PtdIns(3)P in plant cells and the stability of three RxLR (containing the characteristic amino-terminal motif of arginine-X-leucine-arginine, X is any amino acid) effectors. Furthermore, NbVPS15, -30 and -34 were essential for autolysosome formation during Phytophthora capsici infection and limiting programmed cell death (PCD) induced by effectors and elicitors. Taken together, these findings suggest that NbVPS15 and NbVPS34 play a critical role in the resistance of N. benthamiana to Phytophthora pathogens by regulating PtdIns(3)P contents and host PCD.