Nitric oxide mediates the fungal elicitor-induced puerarin biosynthesis in Pueraria thomsonii Benth. suspension cells through a salicylic acid (SA)-dependent and a jasmonic acid (JA)-dependent signal pathway

2006 ◽  
Vol 49 (4) ◽  
pp. 379-389 ◽  
Author(s):  
Maojun Xu ◽  
Jufang Dong ◽  
Muyuan Zhu
2000 ◽  
Vol 13 (3) ◽  
pp. 347-351 ◽  
Author(s):  
Dhirendra Kumar ◽  
Daniel F. Klessig

In tobacco, two mitogen-activated protein (MAP) kinases, designated salicylic acid (SA)-induced protein kinase (SIPK) and wounding-induced protein kinase (WIPK) are activated in a disease resistance-specific manner following pathogen infection or elicitor treatment. To investigate whether nitric oxide (NO), SA, ethylene, or jasmonic acid (JA) are involved in this phenomenon, the ability of these defense signals to activate these kinases was assessed. Both NO and SA activated SIPK; however, they did not activate WIPK. Additional analyses with transgenic NahG tobacco revealed that SA is required for the NO-mediated induction of SIPK. Neither JA nor ethylene activated SIPK or WIPK. Thus, SIPK may function downstream of SA in the NO signaling pathway for defense responses, while the signals responsible for resistance-associated WIPK activation have yet to be determined.


Molecules ◽  
2019 ◽  
Vol 24 (8) ◽  
pp. 1462
Author(s):  
Jie Zhou ◽  
Zhi-fang Ran ◽  
Xiao-tong Yang ◽  
Jia Li

The study highlights the influence and signal transduction mechanism of postharvest UV-B on the production of Rg1 in Panax quinquefolius roots during the drying process. The results showed that postharvest UV-B irradiation induced generation of nitric oxide (NO), jasmonic acid (JA), and ginsenoside Rg1 of P. quinquefolius roots. The UV-B-induced increase of Rg1 was suppressed by NO-specific scavenger (cPTIO) and NOS inhibitors (PBITU), JA synthesis inhibitor (SHAM), and JA synthesis inhibitor (PrGall), indicating that NO and JA played essential parts in UV-B-induced Rg1. External NO inhibitors treatment inhibited UV-B-induced accumulation of NO and JA, which suggested that NO was located upstream of the JA signal pathway. NO-caused Rg1 was inhibited by SHAM and PrGall, implying JA participated in transmitting signal NO to Rg1 accumulation. In other words, NO mediated the postharvest UV-B-induced Rg1 accumulation by the JA-dependent pathway in P. quinquefolius roots during the drying process, which helps us understand the underlying mechanisms involved in UV-B-induced Rg1 production and provides information helpful for P. quinquefolius production.


2013 ◽  
Vol 4 ◽  
Author(s):  
Luis A. J. Mur ◽  
Elena Prats ◽  
Sandra Pierre ◽  
Michael A. Hall ◽  
Kim H. Hebelstrup

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.


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