scholarly journals Tiadinil, a Novel Class of Activator of Systemic Acquired Resistance, Induces Defense Gene Expression and Disease Resistance in Tobacco

2004 ◽  
Vol 29 (1) ◽  
pp. 46-49 ◽  
Author(s):  
Michiko Yasuda ◽  
Hideo Nakashita ◽  
Shigeo Yoshida
2012 ◽  
Vol 25 (9) ◽  
pp. 1209-1218 ◽  
Author(s):  
Xudong Zhang ◽  
Zhonglin Mou

Plant systemic acquired resistance (SAR) is a long-lasting, broad-spectrum immune response that is mounted after primary pathogen infection. Although SAR has been extensively researched, the molecular mechanisms underlying its activation have not been completely understood. We have previously shown that the electron carrier NAD(P) leaks into the plant extracellular compartment upon pathogen attack and that exogenous NAD(P) activates defense gene expression and disease resistance in local treated leaves, suggesting that extracellular NAD(P) [eNAD(P)] might function as a signal molecule activating plant immune responses. To further establish the function of eNAD(P) in plant immunity, we tested the effect of exogenous NAD(P) on resistance gene-mediated hypersensitive response (HR) and SAR. We found that exogenous NAD(P) completely suppresses HR-mediated cell death but does not affect HR-mediated disease resistance. Local application of exogenous NAD(P) is unable to induce SAR in distal tissues, indicating that eNAD(P) is not a sufficient signal for SAR activation. Using transgenic Arabidopsis plants expressing the human NAD(P)-metabolizing ectoenzyme CD38, we demonstrated that altering eNAD(P) concentration or signaling compromises biological induction of SAR. This result suggests that eNAD(P) may play a critical signaling role in activation of SAR.


1998 ◽  
Vol 11 (7) ◽  
pp. 643-658 ◽  
Author(s):  
Shericca W. Morris ◽  
Bernard Vernooij ◽  
Somkiat Titatarn ◽  
Mark Starrett ◽  
Steve Thomas ◽  
...  

Systemic acquired resistance (SAR) is a widely distributed plant defense system that confers broad-spectrum disease resistance and is accompanied by coordinate expression of the so-called SAR genes. This type of resistance and SAR gene expression can be mimicked with chemical inducers of resistance. Here, we report that chemical inducers of resistance are active in maize. Chemical induction increases resistance to downy mildew and activates expression of the maize PR-1 and PR-5 genes. These genes are also coordinately activated by pathogen infection and function as indicators of the defense reaction. Specifically, after pathogen infection, the PR-1 and PR-5 genes are induced more rapidly and more strongly in an incompatible than in a compatible interaction. In addition, we show that monocot lesion mimic plants also express these defense-related genes and that they have increased levels of salicylic acid after lesions develop, similar to pathogen-infected maize plants. The existence of chemically inducible disease resistance and PR-1 and PR-5 gene expression in maize indicates that maize is similar to dicots in many aspects of induced resistance. This reinforces the notion of an ancient plant-inducible defense pathway against pathogen attack that is shared between monocots and dicots.


1996 ◽  
Vol 8 (4) ◽  
pp. 629-643 ◽  
Author(s):  
J Görlach ◽  
S Volrath ◽  
G Knauf-Beiter ◽  
G Hengy ◽  
U Beckhove ◽  
...  

2008 ◽  
Vol 98 (11) ◽  
pp. 1226-1232 ◽  
Author(s):  
M. A. B. Herman ◽  
J. K. Davidson ◽  
C. D. Smart

Plant activators provide an appealing management option for bacterial diseases of greenhouse-grown tomatoes. Two types of plant activators, one that induces systemic acquired resistance (SAR) and a second that activates induced systemic resistance (ISR), were evaluated for control of Pseudomonas syringae pv. tomato and effect on plant defense gene activation. Benzothiadiazole (BTH, SAR-inducing compound) effectively reduced bacterial speck incidence and severity, both alone and in combination with the ISR-inducing product. Application of BTH also led to elevated activation of salicylic acid and ethylene-mediated responses, based on real-time polymerase chain reaction analysis of marker gene expression levels. In contrast, the ISR-inducing product (made up of plant growth-promoting rhizobacteria) inconsistently modified defense gene expression and did not provide disease control to the same level as did BTH. No antagonism was observed by combining the two activators as control of bacterial speck was similar to or better than BTH alone.


2018 ◽  
Author(s):  
Aakanksha Wany ◽  
Pradeep K. Pathak ◽  
Alisdair R Fernie ◽  
Kapuganti Jagadis Gupta

AbstractNitrogen (N) is essential for growth, development and defense but, how low N affects defense and the role of Trichoderma in enhancing defense under low nitrate is not known. Low nitrate fed Arabidopsis plants displayed reduced growth and compromised local and systemic acquired resistance responses when infected with both avirulent and virulent Pseudomonas syringae DC3000. These responses were enhanced in the presence of Trichoderma. The mechanism of increased local and systemic acquired resistance mediated by Trichoderma involved increased N uptake and enhanced protein levels via modulation of nitrate transporter genes. The nrt2.1 mutant is compromised in local and systemic acquired resistance responses suggesting a link between enhanced N transport and defense. Enhanced N uptake was mediated by Trichoderma elicited nitric oxide (NO). Low NO producing nia1,2 mutant and nsHb+ over expressing lines were unable to induce nitrate transporters and thereby compromised defense in the presence of Trichoderma under low N suggesting a signaling role of Trichoderma elicited NO. Trichoderma also induced SA and defense gene expression under low N. The SA deficient NahG transgenic line and the npr1 mutant were also compromised in Trichoderma-mediated local and systemic acquired resistance responses. Collectively our results indicated that the mechanism of enhanced plant defense under low N mediated by Trichoderma involves NO, ROS, SA production as well as the induction of NRT and marker genes for systemic acquired resistance.One-sentence summaryTrichoderma enhances local and systemic acquired resistance under low nitrate nutrition


2001 ◽  
Vol 14 (12) ◽  
pp. 1453-1457 ◽  
Author(s):  
Ping He ◽  
Randall F. Warren ◽  
Tiehan Zhao ◽  
Libo Shan ◽  
Lihuang Zhu ◽  
...  

The tomato Pti5 gene encodes a pathogen-inducible ethylene response element-binding protein-like transcription factor that interacts with the disease resistance gene product Pto. Overexpression of Pti5 or Pti5-VP16, a translational fusion with a constitutive transcriptional activation domain, in tomato enhanced resistance to Pseudomonas syringae pv. tomato. Constitutive expression of Pti5 or Pti5-VP16 did not affect the basal level of pathogenesis-related gene expression, but it accelerated pathogen-induced expression of GluB and Catalase. The results demonstrate a positive role of Pti5 in defense gene regulation and disease resistance and suggest that a pathogen-activated posttran-scriptional regulatory step is necessary for the pathogen induction of the defense gene expression.


2004 ◽  
Vol 39 (6) ◽  
pp. 920-932 ◽  
Author(s):  
Fasong Zhou ◽  
Frank L.H. Menke ◽  
Keiko Yoshioka ◽  
Wolfgang Moder ◽  
Yumiko Shirano ◽  
...  

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