Lysine-Rich Polypeptide Modulates Forkhead Box O3 and Phosphoinositide 3-Kinase-Protein Kinase B Pathway To Induce Apoptosis in Breast Cancer.

The PI3K/AKT/FOXO3 pathway is one of the most frequently involved signaling pathways in cancer, including breast cancer. Therefore, we synthesized a novel lysine-rich polypeptide (Lys-PP) using de novo assembly method and evaluated its anticancer effect. We characterized the structural and physicochemical properties of Lys-PP using various techniques. Later, we used integrated approaches such as in silico, in vitro, and in vivo analysis to confirm the anticancer and therapeutic effect of Lys-PP. First, RNA sequencing suggests Lys-PP disrupted the central carbon metabolic pathway through the modulation of prolactin signaling. Additionally, docking analysis also confirmed the significant association of PI3K/AKT and FOXO3 pathway to induce an apoptotic effect on cancer. Second, Lys-PP exhibited a significant cytotoxicity effect against MDA-MB-231 but no cytotoxic effects on RAW 264.7 and HEK-293, respectively. The cytotoxic effect of Lys-PP-induced apoptosis by an increase in FOXO3a protein expression and a decrease in PI3K/AKT pathway was confirmed by quantitative real-time polymerase chain reaction, immunoblotting, and fluorescent microscopy. Later, immunohistochemistry and hematoxylin and eosin staining on MDA-MD-231 showed increased FOXO3a expression and cell death in the xenograft mice model. Further, liver function, metabolic health, or lipid profile upon Lys-PP showed the absence of significant modulation in the biomarkers except for kidney-related biomarkers. Overall, our comprehensive study provides the first evidence of Lys-PP antibreast cancer action, which could serve as a potential treatment in an alternative or complementary medicine practice.

Coprisin/Compound K Conjugated Gold Nanoparticles Induced Cell Death through Apoptosis and Ferroptosis Pathway in Adenocarcinoma Gastric Cells.

Ferroptosis and apoptosis are programmed cell death pathways with distinct characteristics. Sometimes, cancer cells are aided by the induction of a different pathway, such as ferroptosis, when they develop chemoresistance and avoid apoptosis. Identifying the nanomedicine that targets dual pathways is considered as one of the best strategies for diverse cancer types. In our previous work, we synthesized gold nanoparticles (GNP) utilizing Gluconacetobacter liquefaciens in conjunction with compound K (CK) and coprisin (CopA3), yielding GNP-CK-CopA3. Here, we assessed the inhibitory effect of GNP-CK-CopA3 on AGS cells and the induction of apoptosis using Hoechst and PI, Annexin V-FITC/PI, and qRT-PCR. Subsequently, we conducted downstream proteomic analysis and molecular dynamic stimulation to identify the underlying molecular mechanisms. Our investigation of cultured AGS cells treated with varying concentrations of GNP-CK-CopA3 demonstrated the anticancer properties of these nanoparticles. Penetration of GNP-CK-CopA3 into AGS cells was visualized using an enhanced dark field microscope. Apoptosis induction was initially confirmed by treating AGS cells with GNP-CK-CopA3, as evidenced by staining with dyes such as Hoechst and PI. Additionally, mitochondrial disruption and cellular localization induced by GNP-CK-CopA3 were validated through Mito-tracker staining and transmission electron microscopy images. Annexin V-FITC/PI staining was used to distinguish early and late-stage apoptosis or necrosis based on fluorescence patterns. The gene expression of apoptotic markers indicated the initiation of cellular apoptosis. Further, proteomic analysis suggested that the treatment of GNP-CK-CopA3 to AGS cells led to the suppression of 439 proteins and the stimulation of 832 proteins. Among these, ferroptosis emerged as a significant interconnected pathway where glutathione peroxidase 4 (GPX4) and glutathione synthetase (GSS) were significant interacting proteins. Molecular docking and dynamic simulation studies confirmed the binding affinity and stability between CopA3 and CK with GSS and GPX4 proteins, suggesting the role of GNP-CK-CopA3 in ferroptosis induction. Overall, our study showed GNP-CK-CopA3 could play a dual role by inducing apoptosis and ferroptosis to induce AGS cell death.

A robust high-throughput functional screening assay for plant pathogen effectors using the TMV-GFP vector.

Uncovering the function of phytopathogen effectors is crucial for understanding mechanisms of pathogen pathogenicity and for improving our ability to protect plants from diseases. An increasing number of effectors have been predicted in various plant pathogens. Functional characterization of these effectors has become a major focus in the study of plant-pathogen interactions. In this study, we designed a novel screening system that combines the TMV (tobacco mosaic virus)-GFP vector and Agrobacterium-mediated transient expression in the model plant Nicotiana benthamiana. This system enables the rapid identification of effectors that interfere with plant immunity. The biological function of these effectors can be easily evaluated by observing the GFP fluorescence signal using a UV lamp within just a few days. To evaluate the TMV-GFP system, we initially tested it with well-described virulence and avirulence type III effectors from the bacterial pathogen Ralstonia solanacearum. After proving the accuracy and efficiency of the TMV-GFP system, we successfully screened a novel virulence effector, RipS1, using this approach. Furthermore, using the TMV-GFP system, we reproduced consistent results with previously known cytoplasmic effectors from a diverse array of pathogens. Additionally, we demonstrated the effectiveness of the TMV-GFP system in identifying apoplastic effectors. The easy operation, time-saving nature, broad effectiveness, and low technical requirements of the TMV-GFP system make it a promising approach for high-throughput screening of effectors with immune interference activity from various pathogens.

Genetic Diversity of Ralstonia solanacearum Causing Tobacco Bacterial Wilt in Fujian Province and Identification of Biocontrol Streptomyces sp.

Tobacco bacterial wilt is a highly destructive soilborne disease caused by the Ralstonia solanacearum species complex, exhibiting a significant risk to global flue-cured tobacco cultivation and resulting in substantial economic loss. In this study, 77 isolates were collected from three prominent flue-cured tobacco cultivation areas in Fujian, China (Nanping, Sanming, and Longyan), in 2021 and 2022. The isolated strains were classified through phylotype-specific multiplex polymerase chain reaction (Pmx-PCR) and physiological tests. The analysis showed that all the strains were associated with phylotype I, race 1, and biovar III. Subsequent phylogenetic analysis using partial egl gene sequences classified the 77 isolates into 5 distinct sequevars: 13, 15, 16, 17, and 34. Notably, a remarkable predominance of sequevar 15 was observed in Fujian Province, while sequevar 16 was first reported on tobacco in China, which was identified in other plants, expanding the understanding of its host range and distribution in the country. In addition, a Streptomyces strain extracted from the rhizosphere soil of tobacco was found to inhibit the growth of multiple sequevars of tobacco R. solanacearum, indicating its broad-spectrum antagonistic properties. Furthermore, pot experiments showed that the strain St35 effectively controlled tobacco bacterial wilt. The isolate St35 was conclusively identified as Streptomyces gancidicus according to the morphological and genetic features. In summary, the present study demonstrated the genetic diversity and distribution of tobacco R. solanacearum strains in the Fujian province of China, as well as the identification of a candidate biological control agent for the management of tobacco bacterial wilt.

Comparative anti-inflammatory effect of extract from novel Korean strawberry cultivars (Fragaria × ananassa) on lipopolysaccharide-induced RAW264.7 macrophages and mouse model.

BACKGROUND: Dietary interventions are crucial in modulating inflammation in humans. Strawberries are enjoyed by people of different ages as a result of their attractive phenotype and taste. In addition, the active compounds in strawberries may contribute to the reduction of inflammation. When developing new strawberry cultivars to address agricultural and environmental threats, the bioactivity of strawberries must be improved to maintain their health benefits. RESULTS: We determined the phytochemical contents of extracts from a new Korean strawberry cultivar, with the CN7 cultivar extract possessing the highest total polyphenol and flavonoid contents compared to the CN5 and Seolhyang cultivar extracts. The new Korean strawberry cultivars reduced the expression of inflammatory-related genes in lipopolysaccharide (LPS)-induced RAW264.7 cells via the nuclear factor-kappa B signaling pathway, indicating an anti-inflammatory effect. The CN7 cultivar showed greater bioactivity potential and the highest ellagic acid content; hence, we assessed the effect of the CN7 cultivar in an LPS-stimulated mouse model. The CN7 cultivar treatment demonstrated its effectiveness in reducing inflammation via the downregulation of inflammatory cytokines secretion and gene expression. CONCLUSION: The results obtained in the present study have revealed the observable differences of the newly developed strawberry cultivars with Seolhyang in mitigating inflammation induced by LPS. The enhanced phytochemical content of the CN7 cultivar extract may contribute to its improved anti-inflammatory effect. Therefore, it is crucial to maintain the nutritive benefits of strawberry during the development of new cultivation. © 2023 Society of Chemical Industry.

The anti-inflammation and skin-moisturizing effects of Boehmeria tricuspis-mediated biosynthesized gold nanoparticles in human keratinocytes.

Introduction: Recently, nanotechnology has emerged as a potential technique for skin generation, which has several treatment advantages, such as decreased drug cytotoxicity and enhanced skin penetration. Boehmeria tricuspis (BT) belongs to the Urticaceae family and is rich in phenolic and flavonoid compounds. In this study, we biosynthesized gold nanoparticles (BT-AuNPs) using BT extract to explore their anti-inflammatory and skin-moisturizing properties in keratinocytes. Methods: Field-emission transmission electron microscopy, energydispersive X-ray spectrometry, dynamic light scattering, and Fourier-transforminfrared spectroscopy were used to examine the synthesized BT-AuNPs. qRT-PCR, western blot, and ELISA were applied for investigating the effect of BT-AuNPs on anti-inflammation and moisturizing activity in HaCaT cells. Results: At concentrations below 200 µg/mL, BT-AuNPs had no cytotoxic effect on keratinocytes. BT-AuNPs dramatically alleviated the expression and secretion of inflammatory chemokines/cytokine, such as IL-6, IL-8, TARC, CTACK, and RANTES in keratinocytes stimulated by tumor necrosis factor-α/interferon-γ (T + I). These anti-inflammatory properties of BT-AuNPs were regulated by inhibiting the NF-κB and MAPKs signaling pathways. Furthermore, BT-AuNPs greatly promoted hyaluronic acid (HA) production by enhancing the expression of hyaluronic acid synthase genes (HAS1, HAS2, and HAS3) and suppressing the expression of hyaluronidase genes (HYAL1 and HYAL2) in HaCaT cells. Discussion: These results suggest that BT-AuNPs can be used as a promising therapeutic alternative for treating skin inflammation. Our findings provide a potential platform for the use of BT-AuNPs as candidates for treating inflammatory skin diseases and promoting skin health.

Ubiquitin E3 ligase activity of Ralstonia solanacearum effector RipAW is not essential for induction of plant defense in Nicotiana benthamiana.

As one of the most destructive bacterial phytopathogens, Ralstonia solanacearum causes substantial annual yield losses of many important crops. Deciphering the functional mechanisms of type III effectors, the crucial factors mediating R. solanacearum-plant interactions, will provide a valuable basis for protecting crop plants from R. solanacearum. Recently, the NEL (novel E3 ligase) effector RipAW was found to induce cell death on Nicotiana benthamiana in a E3 ligase activity-dependent manner. Here, we further deciphered the role of the E3 ligase activity in RipAW-triggered plant immunity. We found that RipAWC177A, the E3 ligase mutant of RipAW, could not induce cell death but retained the ability of triggering plant immunity in N. benthamiana, indicating that the E3 ligase activity is not essential for RipAW-triggered immunity. By generating truncated mutants of RipAW, we further showed that the N-terminus, NEL domain and C-terminus are all required but not sufficient for RipAW-induced cell death. Furthermore, all truncated mutants of RipAW triggered ETI immune responses in N. benthamiana, confirming that the E3 ligase activity is not essential for RipAW-triggered plant immunity. Finally, we demonstrated that RipAW- and RipAWC177A-triggered immunity in N. benthamiana requires SGT1 (suppressor of G2 allele of skp1), but not EDS1 (enhanced disease susceptibility), NRG1 (N requirement gene 1), NRC (NLR required for cell death) proteins or SA (salicylic acid) pathway. Our findings provide a typical case in which the effector-induced cell death can be uncoupled with immune responses, shedding new light on effector-triggered plant immunity. Our data also provide clues for further in-depth study of mechanism underlying RipAW-induced plant immunity.

8-paradol from ginger exacerbates PINK1/Parkin mediated mitophagy to induce apoptosis in human gastric adenocarcinoma.

Gastric cancer (GC) occurs in the gastric mucosa, and its high morbidity and mortality make it an international health crisis. Therefore, novel drugs are needed for its treatment. The use of natural products and their components in cancer treatments has shown promise. Therefore, this study aimed to evaluate the effect of 8-paradol, a phenolic compound isolated from ginger (Zingiber officinale Roscoe), on GC and determine its underlying mechanisms of action. In this study, repeated column chromatography was conducted on ginger EtOH extract to isolate gingerol and its derivatives. The cytotoxicity of the eight ginger compounds underwent a (3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide) tetrazolium reduction (MTT) assay. 8-paradol showed the most potent cytotoxicity effect among the isolated ginger compounds. The underlying mechanism by which 8-paradol regulated specific proteins in AGS cells was evaluated by proteomic analysis. To validate the predicted mechanisms, AGS cells and thymus-deficient nude mice bearing AGS xenografts were used as in vitro and in vivo models of GC, respectively. The results showed that the 8-paradol promoted PINK1/Parkin-associated mitophagy, mediating cell apoptosis. Additionally, the inhibition of mitophagy by chloroquine (CQ) ameliorated 8-paradol-induced mitochondrial dysfunction and apoptosis, supporting a causative role for mitophagy in the 8-paradol-induced anticancer effect. Molecular docking results revealed the molecular interactions between 8-paradol and mitophagy-/ apoptosis-related proteins at the atomic level. Our study provides strong evidence that 8-paradol could act as a novel potential therapeutic agent to suppress the progression of GC by targeting mitophagy pathway.

Biologically synthesized black ginger-selenium nanoparticle induces apoptosis and autophagy of AGS gastric cancer cells by suppressing the PI3K/Akt/mTOR signaling pathway.

BACKGROUND: Despite being a promising strategy, current chemotherapy for gastric cancer (GC) is limited due to adverse side effects and poor survival rates. Therefore, new drug-delivery platforms with good biocompatibility are needed. Recent studies have shown that nanoparticle-based drug delivery can be safe, eco-friendly, and nontoxic making them attractive candidates. Here, we develop a novel selenium-nanoparticle based drug-delivery agent for cancer treatment from plant extracts and selenium salts. RESULTS: Selenium cations were reduced to selenium nanoparticles using Kaempferia parviflora (black ginger) root extract and named KP-SeNP. Transmission electron microscopy, selected area electron diffraction, X-ray diffraction, energy dispersive X-ray, dynamic light scattering, and Fourier-transform infrared spectrum were utilized to confirm the physicochemical features of the nanoparticles. The KP-SeNPs showed significant cytotoxicity in human gastric adenocarcinoma cell (AGS cells) but not in normal cells. We determined that the intracellular signaling pathway mechanisms associated with the anticancer effects of KP-SeNPs involve the upregulation of intrinsic apoptotic signaling markers, such as B-cell lymphoma 2, Bcl-associated X protein, and caspase 3 in AGS cells. KP-SeNPs also caused autophagy of AGS by increasing the autophagic flux-marker protein, LC3B-II, whilst inhibiting autophagic cargo protein, p62. Additionally, phosphorylation of PI3K/Akt/mTOR pathway markers and downstream targets was decreased in KP-SeNP-treated AGS cells. AGS-cell xenograft model results further validated our in vitro findings, showing that KP-SeNPs are biologically safe and exert anticancer effects via autophagy and apoptosis. CONCLUSIONS: These results show that KP-SeNPs treatment of AGS cells induces apoptosis and autophagic cell death through the PI3K/Akt/mTOR pathway, suppressing GC progression. Thus, our research strongly suggests that KP-SeNPs could act as a novel potential therapeutic agent for GC.

Biologically Synthesized Rosa rugosa-Based Gold Nanoparticles Suppress Skin Inflammatory Responses via MAPK and NF-κB Signaling Pathway in TNF-α/IFN-γ-Induced HaCaT Keratinocytes.

Nanotechnology-applied materials and related therapeutics have gained attention for treating inflammatory skin diseases. The beach rose (Rosa rugosa), belonging to the family Rosaceae, is a perennial, deciduous woody shrub endemic to northeastern Asia. In this study, R. rugosa-based gold nanoparticles (RR-AuNPs) were biologically synthesized under optimal conditions to explore their potential as anti-inflammatory agents for treating skin inflammation. The synthesized RR-AuNPs were analyzed using field emission-transmission electron microscopy, energy-dispersive X-ray spectrometry, selected-area electron diffraction, and X-ray diffraction. The uniformly well-structured AuNPs showed near-spherical and polygonal shapes. Cell viability evaluation and optical observation results showed that the RR-AuNPs were absorbed by human keratinocytes without causing cytotoxic effects. The effects of RR-AuNPs on the skin inflammatory response were investigated in human keratinocytes treated with tumor necrosis factor-α/interferon-γ (T + I). The results showed that T + I-stimulated increases in inflammatory mediators, including chemokines, interleukins, and reactive oxygen species, were significantly suppressed by RR-AuNP treatment in a concentration-dependent manner. The western blotting results indicated that the RR-AuNP-mediated anti-inflammatory effects were highly associated with the suppression of inflammatory signaling, mitogen-activated protein kinase, and nuclear factor-κB. These results demonstrate that plant extract-based AuNPs are novel anti-inflammatory candidates for topical application to treat skin inflammation.

Three amino acid residues are required for the recognition of Ralstonia solanacearum RipTPS in Nicotiana tabacum.

Ralstonia solanacearum causes devastating diseases in a wide range of economically important crops. It secretes a large number of virulence factors, also known as effectors, to promote its infection, and some of them are recognized when the host plant contains corresponding resistance genes. In this study we showed that a type III effector RipTPS from the avirulent R. solanacearum strain GMI1000 (RipTPSG) specifically induced cell death in Nicotiana tabacum, but not in Nicotiana benthamiana, whereas the RipTPS homolog in the virulent strain CQPS-1 (RipTPSC) induced cell death in neither N. tabacum nor N. benthamiana. These results indicated that RipTPSG is recognized in N. tabacum. Expression of RipTPSG induced upregulation of hypersensitive response (HR) -related genes in N. tabacum. The virulence of CQPS-1 was reduced when RipTPSG was genetically introduced into CQPS-1, further confirming that RipTPSG functions as an avirulence determinant. Protein sequence alignment indicated that there are only three amino acid polymorphisms between RipTPSG and RipTPSC. Site-directed mutagenesis analyses confirmed that the three amino acid residues are jointly required for the recognition of RipTPSG in N. tabacum. Expression of either RipTPSG or RipTPSC suppressed flg22-triggered reactive oxygen species (ROS) burst in N. benthamiana, suggesting that RipTPS contributes to pathogen virulence. Mutating the conserved residues in RipTPS's trehalose-phosphate synthase (TPS) domain did not block its HR induction and defense suppression activity, indicating that the TPS activity is not required for RipTPS's avirulence and virulence function.

A conserved type III effector RipB is recognized in tobacco and contributes to Ralstonia solanacearum virulence in susceptible host plants.

Ralstonia solanacearum, the causal agent of bacterial wilt, causes devastating diseases in a wide range of plants including potato, tomato, pepper and tobacco. The pathogen delivers approximately 70 type III effectors (T3Es) into plant cells during infection. In this study, we confirmed that a T3E RipB is recognized in tobacco. We further demonstrated that RipB is conserved among R. solanacearum isolates and five different ripB alleles are all recognized in tobacco. The ripB from GMI1000 was transformed into susceptible host Arabidopsis, and a defect in root development was observed in ripB-transgenic plants. Pathogen inoculation assays showed that ripB expression promoted plant susceptibility to R. solanacearum infection, indicating that RipB contributes to pathogen virulence in Arabidopsis. Expression of ripB in roq1 mutant partially suppressed reactive oxygen species production, confirming that RipB interferes with plant basal defense. Interestingly, ripB expression promoted cytokinin-related gene expression in Arabidopsis, suggesting a role of cytokinin signaling pathway in plant-R. solanacearum interactions. Finally, RipB harbors potential 14-3-3 binding motifs, but the associations between RipB and 14-3-3 proteins were undetectable in yeast two-hybrid assay. Together, our results demonstrate that multiple ripB alleles are recognized in Nicotiana, and RipB suppresses basal defense in susceptible host to promote R. solanacearum infection.

Biosynthesis of gold nanoparticles using Nigella sativa and Curtobacterium proimmune K3 and evaluation of their anticancer activity.

In recent times, the development of functionalized nanoparticle methodology for biomedical applications has become a major challenge. In the present study, we prepared a novel gold nanoparticle (AuNP), named Curto-Cumin AuNP (CC-AuNP), using the biosynthetic process involving Nigella sativa (black cumin) seed extract and membrane vesicles isolated from the novel probiotic strain, Curtobacterium proimmune K3. Various spectrometric and microscopic analyses were performed to characterize the physicochemical properties of the nanoparticles. CC-AuNP exhibited significant cytotoxicity against human gastric adenocarcinoma (AGS) cells but not against normal cells. The toxic effects of the nanoparticles were associated with the excessive production of reactive oxygen species (ROS) in damaged mitochondria. Further, we investigated the molecular mechanisms underlying the cytotoxic effect of CC-AuNP. Results showed that except for B cell lymphoma 2 (Bcl-2), the intracellular apoptotic signaling molecules, such as p53, Bcl-associated X protein (Bax), and Caspase 9/Caspase 3 were significantly upregulated in AGS cells. ROS production and alterations in mitochondrial membrane potential were observed in AGS cells treated with CC-AuNP. The activation of autophagy flux-related biomarkers, such as LC3b/a, Beclin-1, p62, and Caspase 8, was confirmed by qPCR and western blotting. Autophagy pathway was suppressed in CC-AuNP-treated AGS cells and could not proceed further to the mature state. This was confirmed by the evaluation of both apoptosis and autophagy signaling pathways using autophagy-induced AGS cells treated with rapamycin, a well-studied autophagy activator. Overall, our results showed that CC-AuNP upregulates apoptotic signaling and suppresses the autophagy-related signaling pathway, and thus has potential as an anticancer agent. To our knowledge, the present study is the first to demonstrate that CC-AuNP may serve as novel therapeutic agent against gastric cancer. Furthermore, our study provides preliminary data which can be used to develop novel anticancer candidates and understand their anticancer mechanisms, and seems to be a good starting point for the development of alternative medications based on CC-AuNP.

Gold Nanoparticles Prepared with Phyllanthus emblica Fruit Extract and Bifidobacterium animalis subsp. lactis Can Induce Apoptosis via Mitochondrial Impairment with Inhibition of Autophagy in the Human Gastric Carcinoma Cell Line AGS.

(1) Background: Nanotechnology is being widely applied for anticancer strategies with few side effects. Nanoparticles (NPs) prepared from natural extracts are promising candidates for cancer treatment because of their unique physicochemical characteristics. This study aimed to prepare gold nanoparticles (AuNPs) from Phyllanthus emblica fruit extract (PEFE) using Bifidobacterium animalis subsp. lactis (B. lactis) and to evaluate their anticancer activity against the human gastric adenocarcinoma cell-line (AGS). (2) Methods: The safety of microbial biosynthesis AuNPs (PEFE-AuNPs) was assessed by evaluating the cytotoxicity. The anticancer activity of PEFE-AuNPs was investigated in AGS cells in terms of apoptosis and autophagy. (3) Results: PEFE-AuNPs exhibited significant cytotoxicity against AGS cells but not against normal cells. The apoptosis induced by PEFE-AuNPs in AGS cells was associated with PTEN-induced kinase 1 (PINK1)-Parkin mediated reduction of mitochondrial membrane potential and activation of intracellular signaling apoptosis pathways. The anticancer activity of PEFE-AuNPs was associated with induction of apoptosis through inhibition of autophagy, downregulation of LC3-II/LC3-I and Beclin-1 expression, and upregulation of p62 expression in AGS cells. (4) Conclusions: This study is the first to demonstrate the anticancer activity of PEFE-AuNPs against AGS cells. Our results provide a good starting point for the development of new anticancer products based on gold nanoparticles of P. emblica fruit extract.

An LRR receptor kinase regulates growth, development and pathogenesis in Phytophthora capsici.

Leucine-rich repeats (LRRs) domain containing kinase proteins (LRR-RK) perform various functions in eukaryotic organisms. However, their functions in Oomycetes are still largely unknown. Here, we identified an LRR-RK (PcLRR-RK1) gene and characterized its functions in Phytophthora capsici, a model oomycete specie and a major plant destroyer of solanaceous and cucurbitaceous vegetable crops. We showed that PcLRR-RK1-silenced P. capsici transformants exhibited reduced growth and produced highly branched fluffy hyphae. The shape and size of sporangia were also altered along with the reduced production of number of sporangia and zoospores. Moreover, silencing of the gene affected the cyst germination and penetration of germ tube into the host tissues, and led to the reduced virulence of P. capsici. Thus, we suggest that PcLRR-RK1 was essentially required for zoospores development, and successful infection of the P. capsici.