scholarly journals Foliar Application of Silicon Enhances Resistance Against Phytophthora infestans Through the ET/JA- and NPR1- Dependent Signaling Pathways in Potato

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaojing Xue ◽  
Tiantian Geng ◽  
Haifeng Liu ◽  
Wei Yang ◽  
Weiran Zhong ◽  
...  
Keyword(s):  
Phytophthora Infestans ◽  
Signaling Pathways ◽  
Fungal Pathogens ◽  
Molecular Mechanisms ◽  
Foliar Application ◽  
Dependent Manner ◽  
Virus Induced Gene Silencing ◽  
Detached Leaves ◽  
Oomycete Pathogen ◽  
Ja Signaling

Late blight (LB), caused by the oomycete pathogen Phytophthora infestans, is a devastating disease of potato that is necessary to control by regularly treatment with fungicides. Silicon (Si) has been used to enhance plant resistance against a broad range of bacterial and fungal pathogens; however, the enhanced LB resistance and the molecular mechanisms involving the plant hormone pathways remain unclear. In this study, Si treatment of potato plants was found to enhance LB resistance in both detached leaves and living plants accompanied by induction of reactive oxygen species (ROS) production and pathogenesis-related genes expression. Regarding the hormone pathways involved in Si-mediated LB resistance, we found a rapidly increased content of ethylene (ET) 15 min after spraying with Si. Increased jasmonic acid (JA) and JA-Ile and decreased salicylic acid (SA) were identified in plants at 1 day after spraying with Si and an additional 1 day after P. infestans EC1 infection. Furthermore, pretreatment with Me-JA enhanced resistance to EC1, while pretreatment with DIECA, an inhibitor of JA synthesis, enhanced the susceptibility and attenuated the Si-mediated resistance to LB. Consistent with these hormonal alterations, Si-mediated LB resistance was significantly attenuated in StETR1-, StEIN2-, StAOS-, StOPR3-, StNPR1-, and StHSP90-repressed plants but not in StCOI1- and StSID2-repressed plants using virus-induced gene silencing (VIGS). The Si-mediated accumulation of JA/JA-Ile was significantly attenuated in StETR1-, StEIN2-, StOPR3- and StHSP90-VIGS plants but not in StCOI1-, StSID2- and StNPR1-VIGS plants. Overall, we reveal that Si can be used as a putative alternative to fungicides to control LB, and conclude that Si-mediated LB resistance is dependent on the ET/JA-signaling pathways in a StHSP90- and StNPR1-dependent manner.

The molecular mechanisms of Phytophthora infestans in response to reactive oxygen species (ROS) stress

2021 ◽  
Author(s):  
Xiumei Luo ◽  
Tingting Tian ◽  
Maxime Bonnave ◽  
Xue Tan ◽  
Xiaoqing Huang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Late Blight ◽  
Phytophthora Infestans ◽  
Molecular Mechanisms ◽  
Reactive Oxygen ◽  
Microbial Pathogens ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Tor Signaling ◽  
Potato Resistance

Reactive oxygen species (ROS) are critical for the growth, development, proliferation, and pathogenicity of microbial pathogens; however, excessive levels of ROS are toxic. Little is known regarding the signaling cascades in response to ROS stress in oomycetes such as Phytophthora infestans, the causal agent of potato late blight. Here, P. infestans was used as a model system to investigate the mechanism underlying the response to ROS stress in oomycete pathogens. Results showed severe defects in sporangium germination, mycelial growth, appressorium formation, and virulence of P. infestans in response to H2O2 stress. Importantly, these phenotypes mimic those of P. infestans treated with rapamycin, the inhibitor of target of rapamycin (TOR, 1-phosphatidylinositol-3-kinase). Strong synergism occurred when P. infestans was treated with a combination of H2O2 and rapamycin, suggesting that a crosstalk exists between ROS stress and the TOR signaling pathway. Comprehensive analysis of transcriptome, proteome and phosphorylation omics showed that H2O2 stress significantly induced the operation of the TOR-mediated autophagy pathway. Monodansylcadaverine (MDC) staining showed that in the presence of H2O2 and rapamycin, the autophagosome level increased in a dosage-dependent manner. Furthermore, transgenic potatoes containing double-stranded RNA of PiTOR (TOR in P. infestans) displayed high resistance to P. infestans. Taken together, TOR is involved in the ROS response and is a potential target for control of oomycete diseases, as host-mediated silencing of PiTOR enhances potato resistance to late blight.

Berberine inhibits lipopolysaccharide-induced expression of inflammatory cytokines by suppressing TLR4-mediated NF-ĸB and MAPK signaling pathways in rumen epithelial cells of Holstein calves

2019 ◽  
Vol 86 (2) ◽  
pp. 171-176 ◽  
Author(s):  
Chenxu Zhao ◽  
Yazhou Wang ◽  
Xue Yuan ◽  
Guoquan Sun ◽  
Bingyu Shen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Dependent Manner ◽  
Inflammatory Drug ◽  
Anti Inflammatory ◽  
Mapk Signaling Pathways ◽  
Rumen Epithelial Cells

AbstractSubacute ruminal acidosis (SARA) can increase the level of inflammation and induce rumenitis in dairy cows. Berberine (BBR) is the major active component of Rhizoma Coptidis, which is a type of Chinese anti-inflammatory drug for gastrointestinal diseases. The purpose of this study was to investigate the anti-inflammatory effects of BBR on lipopolysaccharide (LPS)-stimulated rumen epithelial cells (REC) and the underlying molecular mechanisms. REC were cultured and stimulated with LPS in the presence or absence of different concentrations of BBR. The results showed that cell viability was not affected by BBR. Moreover, BBR markedly decreased the concentrations and mRNA expression of pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the LPS-treated REC in a dose-dependent manner. Importantly, Western blotting analysis showed that BBR significantly suppressed the protein expression of toll-like receptor 4 (TLR4) and myeloid differentiation primary response protein (MyD88) and the phosphorylation of nuclear factor-κB (NF-κB), inhibitory kappa B (IκBα), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK) in LPS-treated REC. Furthermore, the results of immunocytofluorescence showed that BBR significantly inhibited the nuclear translocation of NF-κB p65 induced by LPS treatment. In conclusion, the protective effects of BBR on LPS-induced inflammatory responses in REC may be due to its ability to suppress the TLR4-mediated NF-κB and MAPK signaling pathways. These findings suggest that BBR can be used as an anti-inflammatory drug to treat inflammation induced by SARA.

scholarly journals Activation of the Transcription Factor GLI1 by WNT Signaling Underlies the Role of SULFATASE 2 as a Regulator of Tissue Regeneration

2013 ◽  
Vol 288 (29) ◽  
pp. 21389-21398 ◽  
Author(s):  
Ikuo Nakamura ◽  
Maite G. Fernandez-Barrena ◽  
Maria C. Ortiz-Ruiz ◽  
Luciana L. Almada ◽  
Chunling Hu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Wnt Signaling ◽  
Cyclin D1 ◽  
Signaling Pathways ◽  
Tissue Regeneration ◽  
Molecular Mechanisms ◽  
Nuclear Translocation ◽  
Hepatocyte Proliferation ◽  
Dependent Manner ◽  
Gli1 Expression

Tissue regeneration requires the activation of a set of specific growth signaling pathways. The identity of these cascades and their biological roles are known; however, the molecular mechanisms regulating the interplay between these pathways remain poorly understood. Here, we define a new role for SULFATASE 2 (SULF2) in regulating tissue regeneration and define the WNT-GLI1 axis as a novel downstream effector for this sulfatase in a liver model of tissue regeneration. SULF2 is a heparan sulfate 6-O-endosulfatase, which releases growth factors from extracellular storage sites turning active multiple signaling pathways. We demonstrate that SULF2-KO mice display delayed regeneration after partial hepatectomy (PH). Mechanistic analysis of the SULF2-KO phenotype showed a decrease in WNT signaling pathway activity in vivo. In isolated hepatocytes, SULF2 deficiency blocked WNT-induced β-CATENIN nuclear translocation, TCF activation, and proliferation. Furthermore, we identified the transcription factor GLI1 as a novel target of the SULF2-WNT cascade. WNT induces GLI1 expression in a SULF2- and β-CATENIN-dependent manner. GLI1-KO mice phenocopied the SULF2-KO, showing delayed regeneration and decreased hepatocyte proliferation. Moreover, we identified CYCLIN D1, a key mediator of cell growth during tissue regeneration, as a GLI1 transcriptional target. GLI1 binds to the cyclin d1 promoter and regulates its activity and expression. Finally, restoring GLI1 expression in the liver of SULF2-KO mice after PH rescues CYCLIN D1 expression and hepatocyte proliferation to wild-type levels. Thus, together these findings define a novel pathway in which SULF2 regulates tissue regeneration in part via the activation of a novel WNT-GLI1-CYCLIN D1 pathway.

scholarly journals A Verticillium dahliae Extracellular Cutinase Modulates Plant Immune Responses

2018 ◽  
Vol 31 (2) ◽  
pp. 260-273 ◽  
Author(s):  
Yue-Jing Gui ◽  
Wen-Qi Zhang ◽  
Dan-Dan Zhang ◽  
Lei Zhou ◽  
Dylan P. G. Short ◽  
...  
Keyword(s):  
Cell Death ◽  
Plant Defense ◽  
Verticillium Dahliae ◽  
Fungal Pathogens ◽  
Sequence Divergence ◽  
Defense Responses ◽  
Carbohydrate Binding ◽  
Dependent Manner ◽  
Virus Induced Gene Silencing ◽  
Plant Defense Responses

Cutinases have been implicated as important enzymes during the process of fungal infection of aerial plant organs. The function of cutinases in the disease cycle of fungal pathogens that invade plants through the roots has been less studied. Here, functional analysis of 13 cutinase (carbohydrate esterase family 5 domain–containing) genes (VdCUTs) in the highly virulent vascular wilt pathogen Verticillium dahliae Vd991 was performed. Significant sequence divergence in cutinase family members was observed in the genome of V. dahliae Vd991. Functional analyses demonstrated that only VdCUT11, as purified protein, induced cell death and triggered defense responses in Nicotiana benthamiana, cotton, and tomato plants. Virus-induced gene silencing showed that VdCUT11 induces plant defense responses in Nicotiana benthamania in a BAK1 and SOBIR-dependent manner. Furthermore, coinfiltration assays revealed that the carbohydrate-binding module family 1 protein (VdCBM1) suppressed VdCUT11-induced cell death and other defense responses in N. benthamiana. Targeted deletion of VdCUT11 in V. dahliae significantly compromised virulence on cotton plants. The cutinase VdCUT11 is an important secreted enzyme and virulence factor that elicits plant defense responses in the absence of VdCBM1.

Molecular Mechanisms of Antitumor Activity of the Selective Inhibitor of Nuclear Export (SINE) CRM1 Antagonist KPT-185 in Mantle Cell Lymphoma.

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 2438-2438
Author(s):  
Yoko Tabe ◽  
Kensuke Kojima ◽  
Linhua Jin ◽  
Takashi Miida ◽  
Sharon Shacham ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Cyclin D1 ◽  
Signaling Pathways ◽  
Nuclear Export ◽  
Molecular Mechanisms ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Dependent Manner ◽  
Antitumor Effects

Abstract Abstract 2438 CRM1, a member of the importin b super family of nuclear transport receptors, functions as a major nuclear export factor by shuttling transcription factors including p53, p21, I-kB, and FOXO3a from nucleus to cytoplasm, thereby preventing their activity. CRM1 is also involved in the transport of rRNA and a certain subset of mRNAs including Cyclin D1. Upregulated CRM1 expression has been reported to correlate with poor prognosis in various hematopoietic malignancies. MCL is a subtype of B-cell lymphoma which is frequently resistant to standard chemotherapy. The t(11,14)(q13;32) translocation of MCL juxtaposes the cyclin D1 gene, and constitutively overexpressed cyclin D1 is believed to be associated with oncogenesis. Additional genetic events such as mutation/overexpression of TP53 have been reported as adverse prognostic indicators. TP53 mutations are rare in typical MCL, although about 30% of aggressive blastoid MCL have mt-TP53. Because of the multiple signaling pathways that are dysregulated in MCL, a novel strategy aimed at restoring multiple anti-oncogenetic pathways, especially targeting p53-independent signaling pathways, is of considerable interest. In this study, we investigated the antitumor effects and molecular mechanisms of the SINE CRM1 antagonist KPT-185 (Karyopharm Therapeutics) in 4 MCL cells with known TP53 mutation status (wt-TP53: JVM2, Z138; mt-TP53: MINO, Jeko-1). Treatment with KPT-185 resulted in reduction of cell proliferation in a concentration-dependent manner without significant differences between wt- and mt-TP53 cells (IC50 at 72hrs by trypan blue exclusion method; 35nM for Z138, 92 nM for JVM2, 96 nM for MINO, 103 nM for Jeko-1). KPT-185 exhibited limited pro- apoptotic activity in the tested MCL cells except Z138 (ED50 at 48hrs by Annexin V positivity; 62 nM for Z138, 910 nM for JVM2, 665 nM for MINO, 618 nM for Jeko-1). We then investigated KPT-185-induced TP53 target gene expression changes (24 genes) by TaqMan low density arrays (TLDA) (Applied Biosystems). In wt-TP53 JVM2 and Z138 cells, KPT-185 (100nM for Z138, MINO, and 500nM for JVM2, Jeko-1) upregulated classical p53 targets such as p21 and MDM2 mRNA (>2.0 fold), while there was no increase in mt-TP53 MINO and Jeko-1 cells. Of note, in both wt- and mt-TP53 cells, KPT-185 upregulated gene expression of PUMA which is a target of FOXO3a, p73 and p53 (3.3 fold for JVM2, 2.5 fold for Z138, 3.3 fold for MINO, 4.8 fold for Jeko-1). Recently, CRM1 has been reported to positively modulate the nuclear export of Cyclin D1 mRNA in a eIF4E-dependent manner. We therefore examined Cyclin D1 protein levels by western blot analysis, and observed significantly high baseline expression of Cyclin D1 in Z-138 cells which are highly sensitive to KPT-185, as compared to less sensitive MCL cells. KPT-185 treatment decreased Cyclin D1 expression in a dose-dependent manner (50nM and 100nM) after 12hrs of treatment accompanied by p21 induction and decreased p-Rb. These findings demonstrate that KPT-185 successfully inhibits CRM1 activity in MCL resulting in inhibition of Cyclin D1 and cell proliferation, and in the p-53-independent upregulation of pro-apoptotic PUMA. In conclusion, CRM1 inhibition by KPT-185 results in cell growth inhibition and in moderate cell death in a TP-53 independent manner. Results also suggest that the sensitivity to KPT-185 in MCL may be dependent on Cyclin D1 expression. Therefore, KPT-185may be an effective agent for the treatment of MCL. Disclosures: Shacham: Karyopharm Therapeutics: Employment. Kauffman:Karyopharm Therapeutics Inc: Employment.

scholarly journals Arabidopsis late blight: Infection of a nonhost plant by Albugo laibachii enables full colonization by Phytophthora infestans

2015 ◽  
Author(s):  
Khaoula Belhaj ◽  
Liliana M. Cano ◽  
David C. Prince ◽  
Ariane Kemen ◽  
Kentaro Yoshida ◽  
...  
Keyword(s):  
Late Blight ◽  
Phytophthora Infestans ◽  
Molecular Mechanisms ◽  
Transcriptional Profiling ◽  
Unexpected Finding ◽  
Potato Plants ◽  
Nonhost Plant ◽  
Gene Expression Dynamics ◽  
Oomycete Pathogen ◽  
Arabidopsis Cells

AbstractThe oomycete pathogen Phytophthora infestans causes potato late blight, and as a potato and tomato specialist pathogen, is seemingly poorly adapted to infect plants outside the Solanaceae. Here, we report the unexpected finding that P. infestans can infect Arabidopsis thaliana when another oomycete pathogen, Albugo laibachii, has colonized the host plant. The behaviour and speed of P. infestans infection in Arabidopsis pre-infected with A. laibachii resemble P. infestans infection of susceptible potato plants. Transcriptional profiling of P. infestans genes during infection revealed a significant overlap in the sets of secreted-protein genes that are induced in P. infestans upon colonisation of potato and susceptible Arabidopsis, suggesting major similarities in P. infestans gene expression dynamics on the two plant species. Furthermore, we found haustoria of A. laibachii and P. infestans within the same Arabidopsis cells. This Arabidopsis - A. laibachii - P. infestans tripartite interaction opens up various possibilities to dissect the molecular mechanisms of P. infestans infection and the processes occurring in co-infected Arabidopsis cells.

scholarly journals Caragana rosea Turcz Methanol Extract Inhibits Lipopolysaccharide-Induced Inflammatory Responses by Suppressing the TLR4/NF-κB/IRF3 Signaling Pathways

Molecules ◽  
2021 ◽  
Vol 26 (21) ◽  
pp. 6660
Author(s):  
Ankita Mitra ◽  
Akash Ahuja ◽  
Laily Rahmawati ◽  
Han Gyung Kim ◽  
Byoung Young Woo ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Methanol Extract ◽  
Inflammatory Responses ◽  
Eastern China ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Raw264.7 Macrophages ◽  
Anti Inflammatory

Caragana rosea Turcz, which belongs to the Leguminosae family, is a small shrub found in Northern and Eastern China that is known to possess anti-inflammatory properties and is used to treat fever, asthma, and cough. However, the underlying molecular mechanisms of its anti-inflammatory effects are unknown. Therefore, we used lipopolysaccharide (LPS) in RAW264.7 macrophages to investigate the molecular mechanisms that underlie the anti-inflammatory activities of a methanol extract of Caragana rosea (Cr-ME). We showed that Cr-ME reduced the production of nitric oxide (NO) and mRNA levels of iNOS, TNF-α, and IL-6 in a concentration-dependent manner. We also found that Cr-ME blocked MyD88- and TBK1-induced NF-κB and IRF3 promoter activity, suggesting that it affects multiple targets. Moreover, Cr-ME reduced the phosphorylation levels of IκBα, IKKα/β and IRF3 in a time-dependent manner and regulated the upstream NF-κB proteins Syk and Src, and the IRF3 protein TBK1. Upon overexpression of Src and TBK1, Cr-ME stimulation attenuated the phosphorylation of the NF-κB subunits p50 and p65 and IRF3 signaling. Together, our results suggest that the anti-inflammatory activity of Cr-ME occurs by inhibiting the NF-κB and IRF3 signaling pathways.

4-Acetylantrocamol LT3, a New Ubiquinone from Antrodia cinnamomea, Inhibits Hepatocellular Carcinoma HepG2 Cell Growth by Targeting YAP/TAZ, mTOR, and WNT/β-Catenin Signaling

2020 ◽  
Vol 48 (05) ◽  
pp. 1243-1261 ◽  
Author(s):  
Yen-Lin Chen ◽  
I-Chuan Yen ◽  
Kuen-Tze Lin ◽  
Feng-Yi Lai ◽  
Shih-Yu Lee
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Growth ◽  
Cell Viability ◽  
Signaling Pathways ◽  
Hepg2 Cell ◽  
Colony Formation ◽  
Molecular Mechanisms ◽  
Binding Motif ◽  
Dependent Manner ◽  
Antrodia Cinnamomea

4-acetylantrocamol LT3 (4AALT3), a new ubiquinone from the mycelium of Antrodia cinnamomea (Polyporaceae), has been recently shown to possess anticancer activity. However, the detailed mechanisms of such action remain unclear. In this study, the molecular mechanisms of 4AALT3 on hepatocellular carcinoma cells (HCC) were investigated. Human hepatocellular carcinoma cell line HepG2 cells were treated with concentrations of 4AALT3. Cell viability, colony formation, and the underlying mechanisms were then analyzed by CCK-8, colony formation, qPCR, and Western blotting assays. We found that 4AALT3 significantly decreased cell viability and colony formation in a dose-dependent manner. Accordingly, 4AALT3 significantly decreased protein levels of cyclin B, E1, D1, and D3, thereby facilitating cell cycle arrest. In addition, 4AALT3 significantly suppressed the nuclear localization of Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ), mammalian target of rapamycin (mTOR), and WNT/[Formula: see text]-catenin signaling pathways, all of which are well-known signaling pathways that contribute to the malignant properties of HCC. These effects are associated with activation of 5′ AMP-activated protein kinase (AMPK) and autophagy. Our findings indicate that 4AALT3 exerts inhibitory effects on HepG2 cell growth via multiple signaling pathways and may be a potential agent for HCC therapy.

scholarly journals Gene Profiling of a Compatible Interaction Between Phytophthora infestans and Solanum tuberosum Suggests a Role for Carbonic Anhydrase

2005 ◽  
Vol 18 (9) ◽  
pp. 913-922 ◽  
Author(s):  
S. Restrepo ◽  
K. L. Myers ◽  
O. del Pozo ◽  
G. B. Martin ◽  
A. L. Hart ◽  
...  
Keyword(s):  
Carbonic Anhydrase ◽  
Phytophthora Infestans ◽  
Polymerase Chain Reaction Analysis ◽  
Gene Profiling ◽  
Differentially Expressed ◽  
Cdna Clones ◽  
Compatible Interaction ◽  
Virus Induced Gene Silencing ◽  
Oomycete Pathogen ◽  
Late Blight Of Potato

Late blight of potato, caused by the oomycete pathogen Phytophthora infestans, is a devastating disease that can cause the rapid death of plants. To investigate the molecular basis of this compatible interaction, potato cDNA microarrays were utilized to identify genes that were differentially expressed in the host during a compatible interaction with P. infestans. Of the 7,680 cDNA clones represented on the array, 643 (12.9%) were differentially expressed in infected plants as compared with mock-inoculated control plants. These genes were classified into eight groups using a nonhierarchical clustering method with two clusters (358 genes) generally down-regulated, three clusters (241 genes) generally up-regulated, and three clusters (44 genes) with a significant change in expression at only one timepoint. Three genes derived from two down-regulated clusters were evaluated further, using reverse transcription real-time polymerase chain reaction analysis. For these analyses, both incompatible and compatible interactions were included to determine if suppression of these genes was specific to compatibility. One gene, plastidic carbonic anhydrase (CA), was found to have a very different expression pattern in compatible vs. incompatible interactions. Virus-induced gene silencing was used to suppress expression of this gene in Nicotiana benthamiana. In CA-silenced plants, the pathogen grew more quickly, indicating that suppression of CA increases susceptibility to P. infestans.

scholarly journals Transcriptome Analysis and RNA Interference Reveal GhGDH2 Regulating Cotton Resistance to Verticillium Wilt by JA and SA Signaling Pathways

2021 ◽  
Vol 12 ◽  
Author(s):  
Xian-Peng Xiong ◽  
Shi-Chao Sun ◽  
Qian-Hao Zhu ◽  
Xin-Yu Zhang ◽  
Feng Liu ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Verticillium Wilt ◽  
Molecular Mechanisms ◽  
Functional Characterization ◽  
Lignin Biosynthesis ◽  
Differentially Expressed ◽  
Multiple Time ◽  
Virus Induced Gene Silencing ◽  
Network Modules ◽  
Multiple Time Points

Verticillium wilt, caused by Verticillium dahliae, is one of the most damaging and widespread soil-borne cotton diseases. The molecular mechanisms underlying the cotton defense against V. dahliae remain largely elusive. Here, we compared the transcriptional differences between Upland cotton cultivars: one highly resistant (HR; Shidalukang 1) and one highly susceptible (HS; Junmian 1). This was done at multiple time points after V. dahliae inoculation, which identified 2010 and 1275 differentially expressed genes (DEGs) in HR and HS, respectively. Plant hormone signal transduction-related genes were enriched in HR, whereas genes related to lignin biosynthesis were enriched in both HR and HS. Weighted gene co-expression network analysis (WGCNA) using the 2868 non-redundant genes differentially expressed between the V. dahliae infected and uninfected samples in HR or HS identified 10 different gene network modules and 22 hub genes with a potential role in regulating cotton defense against V. dahliae infection. GhGDH2, encoding glutamate dehydrogenase (GDH), was selected for functional characterization. Suppressing the expression level of GhGDH2 by virus-induced gene silencing (VIGS) in HS led to inhibition of the salicylic acid (SA) biosynthesis/signaling pathways and activation of the jasmonic acid (JA) biosynthesis/signaling pathways, which resulted in an increase of 42.1% JA content and a reduction of 78.9% SA content in cotton roots, and consequently enhanced V. dahliae resistance. Our finding provides new insights on the molecular mechanisms of cotton resistance to V. dahliae infection and candidate genes for breeding V. dahliae resistance cotton cultivars by genetic modification.

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