Nitric Oxide Signaling System in Plant Innate Immunity - PAMP Signals in Plant Innate Immunity: Signal Perception and Transduction - page 312

corresponding to fructose 1-6 bisphosphatase, one of the major targets of the
thioredoxin system (Polverari et al. 2003 ). Its expression can lead to an increase
in total cellular glutathione, which participates in the redox signaling system
(Voehringer et al. 2000 ). NO activates glutathione-S-reductase and glutathione
peroxidase which are involved in cell death process (Polverari et al. 2003 ).
NO triggers the activation of two ubiquitin conjugating enzymes UBC10 and
Ahus5 (Polverari et al. 2003 ) and ubiquitin system plays an important role host
defense (Bachmair et al. 1990 , 2001a , b ; Schenk et al. 2000 ). NO is involved in
induction of proteins involved in hypersensitive cell death. ATAF2, a protein belong-
ing to the NAC domain protein family, involved in cell death is induced by NO
(Collinge and Boller 2001 ). Caspases are involved in plant cell death and a caspase-
like activity is detectable in hypersensitively reacting cells following treatment with
NO donors (Clarke et al. 2000 ). Specifi c caspase inhibitors suppress NO-induced
cell death (Clarke et al. 2000 ). A gene encoding the cysteine proteinase RD21A is
shown to be induced by NO at 10 min after treatment and the enzyme is involved in
cell death activation in Arabidopsis thaliana (Swidzinski et al. 2002 ).
NO induces key enzymes in the phenylpropanoid pathway. It induces phenylala-
nine ammonia-lyase (PAL) which is the key enzyme in biosynthesis of phenolics
(Neill et al. 2002 ). Transcription of the genes encoding the enzymes cinnamate-4-
hydroxylase (C4H) and PAL has been shown to be induced by NO (Durner et al.
1998 ). C4H transcription increases following SNP (Sodium nitroprusside, a NO
donor) infi ltration (Delledonne et al. 1998 ). These results suggest that NO is
involved in biosynthesis of phenolics. Chalcone synthase (CHS) is involved in the
synthesis of isofl vonoid phytoalexins and its transcription is also modulated by NO
(Delledonne et al. 1998 ). NO is involved in phytoalexin synthesis (Romero-Puertas
et al. 2004 ). It up-regulates phytoalexin production (Modolo et al. 2002 ). NO acti-
vates peroxidases involved in lignifi cation (Huang et al. 2002 ; Polverari et al. 2003 ).
NO triggers several pathogenesis-related protein genes. It also induces the
pathogenesis-related protein gene Pr1 in tobacco (Durner et al. 1998 ). Expression
level of PR-1 gene rises following administration of NO donors or expression of
recombinant NO-synthase in tobacco (Levine et al. 1994 ). NO is capable of induc-
ing expression of the pathogenesis-related protein PR-1 (Neill et al. 2002 ). NO can
activate induction of -1,3-glucanase, the PR-2 protein (Polverari et al. 2003 ).

NO induces Pr3 gene encoding a chitinase (Grün et al. 2006 ). It also induces
various other defense-related proteins including alternative oxidase and glutathione
S-transferase (Huang et al. 2002 ).

β

6.5 Interplay Between NO and Ca 2+ Signaling Systems

NO plays important role in Ca 2+ signaling system (Courtois et al. 2008 ). It modu-
lates the activity of plasma membrane as well as intracellular Ca 2+ -permeable chan-
nels (Besson-Bard et al. 2008a ). Almost all types of Ca 2+ channels appear to be
regulated by NO (Clementi 1998 ). NO released by NO donors induced a transient