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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 broadspectrum 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 defenserelated 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
Pathogen infection
SA
Defense genes
Disease resistance
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.
Pathogen infection
SA
INA
Defense genes
Disease resistance
Benzothiadiazole (BTH)
 BTH also is a activator of the SAR pathway.
 However, BTH treatment induces both PR-1
mRNA accumulation and P. parasitica resistance
in transgenic Arabidopsis expressing nahG gene,
indicating that BTH action does not required SA
accumulation.
Pathogen infection
BTH
SA
INA
Defense genes
Disease resistance
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.
H2O2
BTH
INA
SABP
(SA-binding protein)
Catalase
H2O + O2
Catalase-SA
SA
Defense genes
Disease resistance
(Klessig, Science 1993. 262:1883-6)
 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-)