Roles of Salicylic Acid, Jasmonic Acid, and Ethylene in cpr-Induced Resistance in Arabidopsis

2000 ◽  
Vol 12 (11) ◽  
pp. 2175 ◽  
Author(s):  
Joseph D. Clarke ◽  
Sigrid M. Volko ◽  
Heidi Ledford ◽  
Frederick M. Ausubel ◽  
Xinnian Dong
2018 ◽  
Vol 31 (12) ◽  
pp. 1271-1279 ◽  
Author(s):  
Xiaochen Jia ◽  
Haihong Zeng ◽  
Wenxia Wang ◽  
Fuyun Zhang ◽  
Heng Yin

Chitosan oligosaccharide (COS) is an effective plant immunity elicitor; however, its induction mechanism in plants is complex and needs further investigation. In this study, the Arabidopsis–Pseudomonas syringae pv. tomato DC3000 (hereafter called DC3000) interaction was used to investigate the induction effect and the underlying mechanisms of COS. COS is effective in inducing resistance to DC3000 in Arabidopsis, and our results demonstrate that treatment with COS 3 days before DC3000 inoculation provided the most effective resistance. Disease severity in jar1 (jasmonic acid [JA]-deficient mutant), NahG, and sid2 (salicylic acid [SA]-deficient mutants) suggest both the SA and JA pathways are required for the Arabidopsis response to DC3000. COS pretreatment induced resistance in wild type (WT), jar1, and also, although to a lesser degree, in NahG and sid2 plants, implying that the SA and JA pathways play redundant roles in COS-induced resistance to DC3000. In COS-pretreated plants, expression of genes related to the SA pathway (PR1, PR2, and PR5) and SA content increased in both WT and jar1. Moreover, expression of genes related to the JA pathway (PDF1.2 and VSP2) and JA content both increased in WT and NahG. In conclusion, COS induces resistance to DC3000 in Arabidopsis by activating both SA- and JA-mediated pathways, although SA and JA pathways play redundant roles in this COS-induced resistance.


2019 ◽  
Vol 109 (7) ◽  
pp. 1102-1114 ◽  
Author(s):  
Qiuying Wang ◽  
Xiuling Chen ◽  
Xinfeng Chai ◽  
Dongqi Xue ◽  
Wei Zheng ◽  
...  

Tomato gray mold disease caused by Botrytis cinerea is a serious disease that threatens tomato production around the world. Clonostachys rosea has been used successfully as a biocontrol agent against divergent plant pathogens, including B. cinerea. To understand the signal transduction pathway of C. rosea-induced resistance to tomato gray mold disease, the effects of C. rosea on gray mold tomato leaves along with changes in the activities of three defense enzymes (phenylalanine ammonialyase [PAL], polyphenol oxidase [PPO], and catalase [CAT]), second messengers (nitric oxide [NO], hydrogen peroxide [H2O2], and superoxide anion radical [O2−]), and stress-related genes (mitogen-activated protein kinase [MAPK], WRKY, Lexyl2, and atpA) in four different hormone-deficient (jasmonic acid [JA], ethylene [ET], salicylic acid [SA], and gibberellin) tomato mutants were investigated. The results revealed that C. rosea significantly inhibited the growth of mycelia and spore germination of B. cinerea. Furthermore, it reduced the incidence of gray mold disease, induced higher levels of PAL and PPO, and induced lower levels of CAT activities in tomato leaves. Moreover, it also increased NO, H2O2, and O2− levels and the gene expression levels of WRKY, MAPK, atpA, and Lexyl2. The incidence of gray mold disease in four hormone-deficient mutants was higher than that in the corresponding wild-type tomato plants. Among all of these hormone-deficient tomato mutants, JA had the most significant effect in regulating the different signal molecules. Additional study suggested that JA upregulated the expression of Lexyl2, MAPK, and WRKY but downregulated atpA. Furthermore, JA also enhanced the activity of PAL, PPO, and CAT and the production of NO and H2O2. SA downregulated CAT and PAL, whereas ET upregulated PAL but downregulated CAT. This study is of significance in understanding the regulatory pathways and biocontrol mechanism of C. rosea against B. cinerea.


2014 ◽  
Vol 71 (1) ◽  
pp. 72-82 ◽  
Author(s):  
Abdul Rashid War ◽  
Michael Gabriel Paulraj ◽  
Savarimuthu Ignacimuthu ◽  
Hari Chand Sharma

2000 ◽  
Vol 12 (11) ◽  
pp. 2175-2190 ◽  
Author(s):  
Joseph D. Clarke ◽  
Sigrid M. Volko ◽  
Heidi Ledford ◽  
Frederick M. Ausubel ◽  
Xinnian Dong

2014 ◽  
Vol 104 (12) ◽  
pp. 1283-1288 ◽  
Author(s):  
Dominik K. Großkinsky ◽  
Eric van der Graaff ◽  
Thomas Roitsch

Phytohormones are known as essential regulators of plant defenses, with ethylene, jasmonic acid, and salicylic acid as the central immunity backbone, while other phytohormones have been demonstrated to interact with this. Only recently, a function of the classic phytohormone cytokinin in plant immunity has been described in Arabidopsis, rice, and tobacco. Although interactions of cytokinins with salicylic acid and auxin have been indicated, the complete network of cytokinin interactions with other immunity-relevant phytohormones is not yet understood. Therefore, we studied the interaction of kinetin and abscisic acid as a negative regulator of plant immunity to modulate resistance in tobacco against Pseudomonas syringae. By analyzing infection symptoms, pathogen proliferation, and accumulation of the phytoalexin scopoletin as a key mediator of kinetin-induced resistance in tobacco, antagonistic interaction of these phytohormones in plant immunity was identified. Kinetin reduced abscisic acid levels in tobacco, while increased abscisic acid levels by exogenous application or inhibition of abscisic acid catabolism by diniconazole neutralized kinetin-induced resistance. Based on these results, we conclude that reduction of abscisic acid levels by enhanced abscisic acid catabolism strongly contributes to cytokinin-mediated resistance effects. Thus, the identified cytokinin–abscisic acid antagonism is a novel regulatory mechanism in plant immunity.


Author(s):  
Huaming He ◽  
Jordi Denecker ◽  
Katrien Van Der Kelen ◽  
Patrick Willems ◽  
Robin Pottie ◽  
...  

Abstract Signaling events triggered by hydrogen peroxide (H2O2) regulate plant growth and defense by orchestrating a genome-wide transcriptional reprogramming. However, the specific mechanisms that govern H2O2-dependent gene expression are still poorly understood. Here, we identify the Arabidopsis Mediator complex subunit MED8 as a regulator of H2O2 responses. The introduction of the med8 mutation in a constitutive oxidative stress genetic background (catalase-deficient, cat2) was associated with enhanced activation of the salicylic acid pathway and accelerated cell death. Interestingly, med8 seedlings were more tolerant to oxidative stress generated by the herbicide methyl viologen (MV) and exhibited transcriptional hyperactivation of defense signaling, in particular salicylic acid- and jasmonic acid-related pathways. The med8-triggered tolerance to MV was manipulated by the introduction of secondary mutations in salicylic acid and jasmonic acid pathways. In addition, analysis of the Mediator interactome revealed interactions with components involved in mRNA processing and microRNA biogenesis, hence expanding the role of Mediator beyond transcription. Notably, MED8 interacted with the transcriptional regulator NEGATIVE ON TATA-LESS, NOT2, to control the expression of H2O2-inducible genes and stress responses. Our work establishes MED8 as a component regulating oxidative stress responses and demonstrates that it acts as a negative regulator of H2O2-driven activation of defense gene expression.


2010 ◽  
Vol 23 (5) ◽  
pp. 585-592 ◽  
Author(s):  
Lennart Eschen-Lippold ◽  
Simone Altmann ◽  
Sabine Rosahl

Inducing systemic resistance responses in crop plants is a promising alternative way of disease management. To understand the underlying signaling events leading to induced resistance, functional analyses of plants defective in defined signaling pathway steps are required. We used potato, one of the economically most-important crop plants worldwide, to examine systemic resistance against the devastating late blight pathogen Phytophthora infestans, induced by treatment with dl-β-aminobutyric acid (BABA). Transgenic plants impaired in either the 9-lipoxygenase pathway, which produces defense-related compounds, or the 13-lipoxygenase pathway, which generates jasmonic acid–derived signals, expressed wild-type levels of BABA-induced resistance. Plants incapable of accumulating salicylic acid (SA), on the other hand, failed to mount this type of induced resistance. Consistently, treatment of these plants with the SA analog 2,6-dichloroisonicotinic acid restored BABA-induced resistance. Together, these results demonstrate the indispensability of a functional SA pathway for systemic resistance in potato induced by BABA.


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