scholarly journals VqMYB154 promotes polygene expression and enhances resistance to pathogens in Chinese wild grapevine

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Changyue Jiang ◽  
Dan Wang ◽  
Jie Zhang ◽  
Yan Xu ◽  
Chaohong Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Transcription Factor ◽  
Pseudomonas Syringae ◽  
Regulatory Mechanism ◽  
Stilbene Synthase ◽  
Gus Activity ◽  
Uncinula Necator ◽  
Oxygen Species ◽  
Wild Grapevine

AbstractResveratrol plays a crucial phytoalexin role in the grapevine and is beneficial to human health. However, the molecular mechanism of resveratrol accumulation in the enhancement of disease resistance is unclear. Here, we report that the transcription factor VqMYB154 from Vitis quinquangularis accession Danfeng-2 is strongly expressed under artificial inoculation with Uncinula necator and regulates resveratrol accumulation. Unlike its homolog, VqMYB154 has a pathogen-induced promoter and responds to stimulation by U. necator, Pseudomonas syringae, and other treatments. Yeast one-hybrid and GUS activity assays confirmed that VqMYB154 can activate the stilbene synthase genes VqSTS9, VqSTS32, and VqSTS42 by directly binding to their promoters. Overexpression of VqMYB154 in grape leaves resulted in activation of the stilbene pathway, upregulation of STS genes, and accumulation of stilbenoids. In addition, heterologous overexpression of VqMYB154 in Arabidopsis activated resistance-related genes and resulted in greater programmed cell death and accumulation of reactive oxygen species, which led to resistance against P. syringae. These results suggest that the transcription factor VqMYB154 from V. quinquangularis accession Danfeng-2 participates in the regulatory mechanism that improves the biosynthesis and accumulation of stilbenes and enhances resistance to disease in grapevine.

scholarly journals NTRC and Chloroplast-Generated Reactive Oxygen Species Regulate Pseudomonas syringae pv. tomato Disease Development in Tomato and Arabidopsis

2012 ◽  
Vol 25 (3) ◽  
pp. 294-306 ◽  
Author(s):  
Yasuhiro Ishiga ◽  
Takako Ishiga ◽  
Tamding Wangdi ◽  
Kirankumar S. Mysore ◽  
Srinivasa Rao Uppalapati
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Pseudomonas Syringae ◽  
Function Analysis ◽  
Virulent Strain ◽  
Reactive Oxygen ◽  
Forward Genetics ◽  
Negative Regulator ◽  
Dependent Manner ◽  
Oxygen Species

Coronatine (COR)-producing pathovars of Pseudomonas syringae, including pvs. tomato, maculicola, and glycinea, cause important diseases on tomato, crucifers, and soybean, respectively, and produce symptoms with necrotic lesions surrounded by chlorosis. The chlorosis is mainly attributed to COR. However, the significance of COR-induced chlorosis in localized lesion development and the molecular basis of disease-associated cell death is largely unknown. To identify host (chloroplast) genes that play a role in COR-mediated chlorosis, we used a forward genetics approach using Nicotiana benthamiana and virus-induced gene silencing and identified a gene which encodes 2-Cys peroxiredoxin (Prxs) that, when silenced, produced a spreading hypersensitive or necrosis-like phenotype instead of chlorosis after COR application in a COI1-dependent manner. Loss-of-function analysis of Prx and NADPH-dependent thioredoxin reductase C (NTRC), the central players of a chloroplast redox detoxification system, resulted in spreading accelerated P. syringae pv. tomato DC3000 disease-associated cell death with enhanced reactive oxygen species (ROS) accumulation in a COR-dependent manner in tomato and Arabidopsis. Consistent with these results, virulent strain DC3000 suppressed the expression of Prx and NTRC in Arabidopsis and tomato during pathogenesis. However, interestingly, authentic COR suppressed the expression of Prx and NTRC in tomato but not in Arabidopsis, suggesting that COR in conjunction with other effectors may modulate ROS and cell death in different host species. Taken together, these results indicated that NTRC or Prx function as a negative regulator of pathogen-induced cell death in the healthy tissues that surround the lesions, and COR-induced chloroplast-localized ROS play a role in enhancing the disease-associated cell death.

scholarly journals Cystine and Methionine Deficiency Promotes Ferroptosis by Inducing B-Cell Translocation Gene 1

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1543
Author(s):  
Il-Je Cho ◽  
Doyeon Kim ◽  
Eun-Ok Kim ◽  
Kyung-Hwan Jegal ◽  
Jae-Kwang Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Cell Death ◽  
Transcription Factor ◽  
Stress Response ◽  
B Cell ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Integrated Stress Response ◽  
Methionine Deficiency

Ferroptosis is a type of programmed necrosis triggered by iron-dependent lipid peroxidation. We investigated the role of B-cell translocation gene 1 (BTG1) in cystine and methionine deficiency (CST/Met (–))-mediated cell death. CST/Met (–) depleted reduced and oxidized glutathione in hepatocyte-derived cells, increased prostaglandin-endoperoxide synthase 2 expression, and promoted reactive oxygen species accumulation and lipid peroxidation, as well as necrotic cell death. CST/Met (–)-mediated cell death and lipid peroxidation was specifically inhibited by pretreatment with ferroptosis inhibitors. In parallel with cell death, CST/Met (–) blocked global protein translation and increased the expression of genes associated with the integrated stress response. Moreover, CST/Met (–) significantly induced BTG1 expression. Using a BTG1 promoter-harboring reporter gene and siRNA, activating transcription factor 4 (ATF4) was identified as an essential transcription factor for CST/Met (–)-mediated BTG1 induction. Although knockout of BTG1 in human HAP1 cells did not affect the accumulation of reactive oxygen species induced by CST/Met (–), BTG1 knockout significantly decreased the induction of genes associated with the integrated stress response, and reduced lipid peroxidation and cell death in response to CST/Met (–). The results demonstrate that CST/Met (–) induces ferroptosis by activating ATF4-dependent BTG1 induction.

scholarly journals WRKY55 transcription factor positively regulates leaf senescence and the defense response by modulating the transcription of genes implicated in the biosynthesis of reactive oxygen species and salicylic acid in Arabidopsis

Development ◽  
2020 ◽  
Vol 147 (16) ◽  
pp. dev189647
Author(s):  
Yiqiao Wang ◽  
Xing Cui ◽  
Bo Yang ◽  
Shutao Xu ◽  
Xiangyan Wei ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Transcription Factor ◽  
Salicylic Acid ◽  
Pseudomonas Syringae ◽  
Leaf Senescence ◽  
Single Gene ◽  
Bacterial Pathogen ◽  
Reactive Oxygen ◽  
Pathogen Resistance ◽  
Oxygen Species

ABSTRACTReactive oxygen species (ROS) and salicylic acid (SA) are two factors regulating leaf senescence and defense against pathogens. However, how a single gene integrates both ROS and SA pathways remains poorly understood. Here, we show that Arabidopsis WRKY55 transcription factor positively regulates ROS and SA accumulation, and thus leaf senescence and resistance against the bacterial pathogen Pseudomonas syringae. WRKY55 is predominantly expressed in senescent leaves and encodes a transcriptional activator localized to nuclei. Both inducible and constitutive overexpression of WRKY55 accelerates leaf senescence, whereas mutants delay it. Transcriptomic sequencing identified 1448 differentially expressed genes, of which 1157 genes are upregulated by WRKY55 expression. Accordingly, the ROS and SA contents in WRKY55-overexpressing plants are higher than those in control plants, whereas the opposite occurs in mutants. Moreover, WRKY55 positively regulates defense against P. syringae. Finally, we show that WRKY55 activates the expression of RbohD, ICS1, PBS3 and SAG13 by binding directly to the W-box-containing fragments. Taken together, our work has identified a new WRKY transcription factor that integrates both ROS and SA pathways to regulate leaf senescence and pathogen resistance.

scholarly journals The Pepper Calmodulin Gene CaCaM1 Is Involved in Reactive Oxygen Species and Nitric Oxide Generation Required for Cell Death and the Defense Response

2009 ◽  
Vol 22 (11) ◽  
pp. 1389-1400 ◽  
Author(s):  
Hyong Woo Choi ◽  
Dong Hyuk Lee ◽  
Byung Kook Hwang
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Transient Expression ◽  
Pseudomonas Syringae ◽  
Xanthomonas Campestris ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Defense Responses ◽  
Oxygen Species

Calcium signaling has emerged as an important signal transduction pathway of higher plants in response to biotic and abiotic stresses. Ca2+-bound calmodulin (CaM) plays a critical role in decoding and transducing stress signals by activating specific targets. Here, we isolated and functionally characterized the pathogen-responsive CaM gene, Capsicum annuum calmodulin 1 (CaCaM1), from pepper (C. annuum) plants. The cellular function of CaCaM1 was verified by Agrobacterium spp.-mediated transient expression in pepper and transgenic overexpression in Arabidopsis thaliana. Agrobacterium spp.-mediated transient expression of CaCaM1 activated reactive oxygen species (ROS), nitric oxide (NO) generation, and hypersensitive response (HR)-like cell death in pepper leaves, ultimately leading to local acquired resistance to Xanthomonas campestris pv. vesicatoria. CaCaM1-overexpression (OX) Arabidopsis exhibited enhanced resistance to Pseudomonas syringae and Hyaloperonospora parasitica, which was accompanied by enhanced ROS and NO generation and HR-like cell death. Treatment with the calcium-channel blocker suppressed the oxidative and NO bursts and HR-like cell death that were triggered by CaCaM1 expression in pepper and Arabidopsis, suggesting that calcium influx is required for the activation of CaCaM1-mediated defense responses in plants. Upon treatment with the CaM antagonist, virulent P. syringae pv. tomato-induced NO generation was also compromised in CaCaM1-OX leaves. Together, these results suggest that the CaCaM1 gene functions in ROS and NO generation are essential for cell death and defense responses in plants.

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