Roles of Salicylic Acid, Jasmonic Acid, and Ethylene in cpr-Induced Resistance in Arabidopsis

Abstract

Disease resistance in Arabidopsis is regulated by multiple signal transduction pathways in which salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) function as key signaling molecules. Epistasis analyses were performed between mutants that disrupt these pathways ( npr1 , eds5 , ein2 , and jar1 ) and mutants that constitutively activate these pathways ( cpr1, cpr5 , and cpr6 ), allowing exploration of the relationship between the SA-and JA/ET-mediated resistance responses. Two important findings were made. First, the constitutive disease resistance exhibited by cpr1 , cpr5, and cpr6 is completely suppressed by the SA-deficient eds5 mutant but is only partially affected by the SA-insensitive npr1 mutant. Moreover, eds5 suppresses the SA-accumulating phenotype of the cpr mutants, whereas npr1 enhances it. These data indicate the existence of an SA-mediated, NPR1-independent resistance response. Second, the ET-insensitive mutation ein2 and the JA-insensitive mutation jar1 suppress the NPR1-independent resistance response exhibited by cpr5 and cpr6 . Furthermore, ein2 potentiates SA accumulation in cpr5 and cpr5 npr1 while dampening SA accumulation in cpr6 and cpr6 npr1 . These latter results indicate that cpr5 and cpr6 regulate resistance through distinct pathways and that SA-mediated, NPR1-independent resistance works in combination with components of the JA/ETmediated response pathways. INTRODUCTIONIn plants, resistance to pathogen infection is accomplished through protective physical barriers and a diverse array of antimicrobial chemicals and proteins. Many of these antimicrobial compounds are part of an active defense response, and their rapid induction is contingent on the plant's ability to recognize and respond to an invading pathogen (Staskawicz et al., 1995;Baker et al., 1997). Pathogen recognition often involves the interaction of an avirulence signal (encoded by pathogen avr genes) and cognate plant resistance gene (R) products (Staskawicz et al., 1995;Bent, 1996;Baker et al., 1997). The avr/R interaction often triggers a strong defense mechanism known as the hypersensitive response (HR) (Flor, 1947(Flor, , 1971 Keen, 1990;Van Der Biezen and Jones, 1998). In general, pathogens that activate avr/Rmediated signaling pathways do not cause disease and are said to be avirulent.An HR activated by avr/R signaling is characterized by several physiological changes, including the accumulation of reactive oxygen intermediates, nitric oxide, and salicylic acid (SA) (Dangl et al., 1996; Hammond-Kosack and Jones, 1996; Low and Merida, 1996;Lamb and Dixon, 1997; Delledonne et al., 1998; Durner et al., 1998). Jasmonic acid (JA) and ethylene (ET) are also produced in response to pathogen infection, most probably because of an increase in lipoxygenase and 1-amino-cyclopropane-1-carboxylic acid (ACC) oxidase activities, respectively (Gundlach et al., 1992; HammondKosack et al., 1996; May et al., 1996; Penninckx et al., 1996;Thomma et al., 1998). SA, JA, and ET induce the production of antimicrobial compounds such...

The role of JAR1 in Jasmonoyl-l-isoleucine production during Arabidopsis wound response

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The physiology of ozone induced cell death

“…Earlier studies have assumed that plants induce SA-, JA-, and ethylene-signaling pathways that act linearly and independently, and trigger distinct plant defense responses including cell death. However, studies with various mutants of Arabidopsis revealed that SA-, JA-and ethylene-signaling pathways do not act independently and that plants are equipped with regulatory components to control the magnitude of each of these pathways and to mediate the interactions between these diverse signaling pathways (Dong 1998;Genoud and Metraux 1999;Clarke et al 2000;Greenberg et al 2000;Overmyer et al 2000;Rao et al 2000b;O'Donnell et al 2001). Having shown that acute O 3 exposure triggers plant HR cell death, several laboratories including ours, have used O 3 as an abiotic elicitor of plant HR cell death (reviewed in Rao et al 2000a).…”

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