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

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