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6.10
Role of NO in Salicylic Acid-Regulated Systemic
Acquired Resistance
SA signaling system activates not only local resistance, but also systemic acquired
resistance (SAR) observed in distal (systemic) tissues. SAR is a SA-dependent height-
ened defense to a broad spectrum of pathogens that is activated throughout a plant
following local infection (Liu et al. 2011 ). Infection of plants by necrotizing patho-
gens, which induce the accumulation of SA, or treatment of plants with synthetic
compounds, which are able to trigger SA signaling, causes the induction of a unique
physiological state called “priming” (Slaughter et al. 2012 ). SAR is associated with
priming of defense (Kohler et al. 2002 ; Luna et al. 2011 ) and the priming results in a
faster and stronger induction of defense mechanisms after pathogen attack (Conrath
2011 ). The priming can be inherited epigenetically from disease-exposed plants
(Pastor et al. 2013 ) and descendants of primed plants exhibit next-generation systemic
acquired resistance (Luna et al. 2011 ; Slaughter et al. 2012 ). The transgenerational
SAR has been recently reported (Luna et al. 2011 ).
NPR1 is an important regulator of SAR downstream of SA (Mou et al. 2003 ;
Zhang et al. 2003 ). The events downstream of SA include an increase of NO (Zottini
et al. 2007 ), which may then serve as signaling mediator itself (Krinke et al. 2007 ).
NO is required for the full function of NPR1 in SA-triggered SAR (Song and
Goodman 2001 ). Nuclear localization of NPR1 protein is essential for its function
(Kinkema et al. 2000 ; Meur et al. 2006 ). Without induction, NPR1 protein forms an
oligomer and is excluded from the nucleus. Redox changes cause monomeric NPR1
to emerge and accumulate in the nucleus and activate PR gene expression (Kinkema
et al. 2000 ; Mou et al. 2003 ).
Plant immunity requires conformational changes of NPR1 via S-nitrosylation
and thioredoxin (Tada et al. 2008 ). NPR1 is sequestered in the cytoplasm as an
oligomer through intermolecular disulfi de bonds. NO-mediated S-nitrosylation of
NPR1 by S-nitrosoglutathione (GSNO) at Cys156 facilitates the NPR1 oligomer-
ization, which maintains protein homeostasis upon SA induction. Conversely, the
SA-induced NPR1 oligomer-to-monomer reaction is catalyzed by thioredoxins
(TRX). Mutants in both NPR1 Cys156 and TRX compromised NPR1-mediated
disease resistance response. Thus, the regulation of NPR1 is through opposing
action of NO-dependent GSNO and ROS-dependent TRX (Tada et al. 2008 ). These
results suggest that NO is involved in the action of NPR1 in triggering SAR. It also
has been shown that NO-induced nitrosoglutathione could act as a long-distance
phloematic signal in SAR (Durner and Klessig 1999 ) .
References
Ali R, Ma W, Lemtiri-Chlieh F, Tsaltas D, Leng Q, von Bodman S, Berkowitz GA (2007) Death
don't have no mercy and neither does calcium: Arabidopsis CYCLIC NUCLEOTIDE GATED
CHANNEL2 and innate immunity. Plant Cell 19:1081-1095
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