chapter 10 systemic acquired resistance (sar)
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Chapter 10
Systemic Acquired Resistance (SAR)
Resistance
Race-specific resistance Race-nonspecific resistance
Also called general resistance Nonhost resistance Systemic acquired resistance (SAR)
Systemic Acquired Resistance (SAR)
Many plants infected by a pathogen develop broad-spectrum and systemic resistance against subsequent infection by the same or other pathogens.
For example, TMV inoculation of tobacco “Xanthi”, a local lesion host, leads to enhanced resistance to subsequent challenge with either TMV, Cercospora nicotiana, Phytophthora parasitica, Peronospora tabacina, or Pseudomonas syringae pv. tabaci.
SAR result from increased levels of defense compounds including PR proteins and other defense-related proteins.
The R-avr gene interaction triggers a signal transduction pathway leading to the HR and SAR
What is the endogenous signal responsible for activation of SAR?
Salicyclic acids - the endogenous signal for SAR
SA levels increase in the area of hypersensitive tissues of TMV-inoculated tobacco or TNV- or Colletotrichum lagenarium-inoculated cucumber.
SA can be recovered from phloem, indicating that it can be translocated in plants.
SA treated tobacco or cucumber leaves activate a broad spectrum of defense response.
SA confers the treated plants SAR to subsequent pathogenic infection.
(continued)
Salicyclic acids - the endogenous signal for SAR
Salicylate hydrolase (nahG) catalyze the conversion of salicyclic acid to catechol.
J. Ryals isolated nahG from Pseudomonas putida. Transgenic tobacco plants that express high levels of
salicylate hydrolase are not capable of inducing SAR, while transgenic plants with undetectable levels of the salicylate hydrolase mRNA express SAR.
Thus, SA is a signal molecule for SAR.
(J. Ryals, Ciba-Geigy, 1995. Plant Mol. Bio.)
nahG
SA
Disease resistance
Defense genes
Pathogen infection
Systemic Acquired Resistance (SAR)
Systemic Acquired Resistance (SAR)
SAR may be elicited in Arabidopsis by treatment of salicyclic acid (SA), 2,6-dichloroisonicotinic acid (INA), benzothiadiazole (BTH) or inoculation of an avirulent pathogen.
2,6-dichloroisonicotinic acid (INA)
INA is an activator of the SAR pathway. INA induces expression of the same set of SAR genes
induced by either SA treatment or pathogen infection.
However, no SA accumulation was detected during the time required for the induction of SAR gene expression or disease resistance.
Furthermore, INA induces both resistance and SAR gene expression in transgenic tobacco and Arabidopsis plants that cannot accumulate SA.
Thus, INA apparently activates a component of the SAR signaling pathway which locates at the downstream of SA.
SA
Disease resistance
Defense genes
Pathogen infection
INA
Benzothiadiazole (BTH)
BTH also is a activator of the SAR pathway. However, BTH treatment induces both PR-1 mR
NA accumulation and P. parasitica resistance in transgenic Arabidopsis expressing nahG gene, indicating that BTH action does not required SA accumulation.
SA
Disease resistance
Defense genes
Pathogen infection
INABTH
Involvement of H2O2 in SAR
Elevated level of cellular reactive oxygen species (i.e., H2O2) was observed in plants with SAR.
Chen and Klessig (1993) isolated a SA-binding protein (SABP) from the cDNA library of tobacco leaves.
The deduced cDNA sequence indicates that SABP is a catalase.
They proposed that SA activates the elevated levels of cellular H2O2 by inhibiting the catalase activity.
Cellular H2O2 functions as a secondary messenger in SAR signal transduction.
SABP
CatalaseH2O2 H2O + O2
Catalase-SA
SA
Disease resistance
Defense genes
(Klessig, Science 1993. 262:1883-6)
(SA-binding protein)
INABTH
Catalase isoforms that bind SA have been detected in variety of plants, including tobacco, tomato, cucumber, and Arabidopsis.
H2O2
H2O2
SA
SA
END
Plant defense against pathogens
(A-)
(R-)
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