Recent Advances and Future Prospects on Practical Use of Salicylic Acid - Salicylic Acid: Plant Growth and Development - page 359

NO, O 2 - is scavenged before it is dismutated to H 2 O 2 . Whereas the cooperation of
NO and H 2 O 2 leads to the death of the cell, reciprocal scavenging of NO and O 2 -
leads to the formation of ONOO - , which appears to be non-toxic in plants
(Delledone et al. 2001 ; Zaninotto et al. 2006 ).
Both ROS and SA have been shown to synergize with NO to enhance host cell
death in soybean suspension cells (Delledonne et al. 1998 ). In addition, SA may
mediate and/or potentiate NO's effects by altering the activity of various NO-
regulated enzymes. SA also induces the synthesis of a pathogen-inducible oxy-
genase in plants that has strong homology to a mammalian cyclooxygenase (Sanz
et al. 1998 ). This enzyme is posttranslationally activated by NO in mammals
(Nogawa et al. 1998 ). Thus, SA and NO may work synergistically to transduce the
defense signal by targeting the same effector proteins and/or their genes.
In other cases SA may antagonize the NO signaling pathway. It has been
reported that in plants SA may antagonize NO's ability to inhibit respiration (and
thereby cause oxidative stress) by activating the NO-insensitive alternative oxidase
(Millar and Day 1997 ). Considering the many interactions that are currently
emerging between the pleiotropic effectors SA, NO, and other ROS, it is apparent
that researchers are at a very early stage in understanding the complexity of their
action in disease resistance.
NO also functions independently of ROS in the induction of various defense
genes, including those found in pathogenesis-related proteins and enzymes of
phenylpropanoid metabolism involved in the production of lignin, antibiotics and
the secondary signal salicylic acid. The mobile nature of NO and its chemical
reactivity with various cellular targets means that downstream effects of NO may
be directly induced by interaction with various cellular components, like ion
channels or proteins that modulates gene expression, or indirectly following
interaction with signaling proteins such as protein kinases. NO signaling functions
depend on its reactivity and ROS are key modulators of NO in triggering cell
death, although through mechanisms different from those commonly observed in
animals (Delledonne et al. 2001 ). As ROS initiate various signaling pathways, the
preservation of suitable ROS levels might correspond to survival response. NO
interacts with ROS in different ways and serves as an antioxidant during various
stresses (Wellburn 1990 ). In the pathogen-activated hypersensitive response, both
NO and ROS act as signal molecules (Delledonne 2005 ). ROS and NO are also
involved in the regulation of SA biosynthesis (Durner et al. 1998 ).
Several models suggest that redox signalling through NO and ROS is enhanced
by SA in a self-amplifying process (Klessig et al. 2000 ). Nonetheless, the rela-
tionship between NO, SA, and ROS in the activation of defense genes and/or
induction of host cell death is not clearly defined. Several lines of evidence point
to an inter-relationship between NO and SA in plant defense. It is well documented
that both SA and NO play important role in activation of plant defense responses
after pathogen attacks, but the interrelationship between their respective signaling
pathways is still unclear.
Treatment of tobacco and A. thaliana leaves with NO induces a substantial
increase in endogenous SA (Durner et al. 1998 ). Song and Goodman ( 2001 )