Nitric Oxide Involvement in Incompatible Plant–Pathogen Interactions - Communication in Plants: Neuronal Aspects of Plant Life - page 116

of NO in plant hypersensitive cell death. In A. thaliana suspension cells,
NO donors induce cell death at concentrations similar to those generated
by cells challenged by avirulent bacteria (Clarke et al. 2000). In soybean
cell suspensions, cell death appears to be mediated by relative levels of
NO and H 2 O 2 (Delledonne et al. 2001). The same results were seen in
tobacco cultured cells where the addition of a NO donor and a H 2 O 2 gen-
erator separately had no effect on cell viability. However, when NO and
H 2 O 2 were added simultaneously, cells died in a concentration-dependent
manner (de Pinto et al. 2003). Whereas the mechanism by which NO and
H 2 O 2 interact for killing is still largely unknown, the reaction between NO
and O 2 produces ONOO − (Koppenol et al. 1992), a highly reactive oxidant
molecule that interacts with many molecular components and may mod-
ulate downstream signaling (Beckman et al. 1990). In mammals, ONOO −
induces apoptosis and is also cytotoxic by causing oxidative tissue dam-
age (Lin et al. 1995). In plants ONOO − does not appear to be an essential
intermediate of NO-induced cell death (Delledonne et al. 2001). However,
ONOO − induces PR-1 accumulation in tobacco leaves (Durner and Klessig
1999) and protein nitration leading to changes in the redox state of the cell
(Delledonne et al. 2001).
8.6
NO Signaling in the Plant Defense Response
ThemobilenatureofNOanditschemicalreactivitywithvariouscellular
targets means that the downstream effects of NO may be directly induced by
interaction of NO with various cellular components such as ion channels or
proteins that modulate gene expression, or indirectly following interaction
of NO with signaling proteins (Neill et al. 2003). In mammalian systems, one
of the most important targets of NO is guanylate cyclase (GC). NO interacts
with the heme prosthetic group of this enzyme, leading to its activation and
resultinginanincreasedgenerationofintracellularcyclicGMP(cGMP).In
plants, a similar activation of GC has also been suggested (Hancock et al.
2002). Administration of NO donors or recombinant mammalian NOS to to-
bacco plants or suspension cells triggers the expression of PR-1 and pheny-
lalanine ammonia lyase (PAL) (Durner and Klessig 1999). These genes are
also induced by cGMP, suggesting that the NO/cGMP-dependent signaling
pathway present in animals may also exist in plants. In addiction, two in-
hibitors of NO-inducible GC are able to suppress induction of PAL in tobacco
plants, suggesting the involvement of cGMP-dependent components in NO-
dependent defense gene activation. However GC inhibitors produced only
a partial suppression of PAL transcripts, suggesting the existence of both
cGMP-dependent and cGMP-independent pathways (Durner et al. 1998).