of Atractylodes lancea. Furthermore pretreatment of plantlets with exogenous
NO donor promoted volatile oil accumulation, while treatment with NO scavenger
inhibited the burst of salicylic acid and volatile oil accumulation induced by the
fungus. Likewise elicitation with another endophytic fungal Cunninghamella sp.
also induced the NO-mediated accumulation of atractylone, hinesol, β-eudesmol,
and atractylodin in suspension cells of A. lancea [104]. NO induced by cerebroside
elicitor from Fusarium was involved in the regulation of artemisinin production by
increasing the gene expression of 1-deoxy-D-xylulose 5-phosphate synthase and
hydroxybenzoate meta-geranyltransferase in A. annua hairy roots as well [102]. It
was reported that oligogalacturonic acid-induced NO accumulation could improve
the transcription of squalene synthase and squalene epoxidase, two early enzymes
for the synthesis of triterpenoid saponins in cell cultures of Panax ginseng [121].
Similarly, NO burst followed by the biosynthesis of torpinoid β-thujaplicin in
elicited Cupressus lusitanica cells which has strong antifungal, antiviral, and anticancer activities [126]. NO was found to reduce the transcription of genes in the
monoterpenoid indole alkaloids pathway and the octadecanoid-responsive
Catharanthus AP2/ERF domain transcription through the inhibition of type-I protein prenyltransferase gene, leading to a downregulation of the catharanthine biosynthesis [96].
NO may also interact with other signaling molecules integral of plant defense
system including jasmonic acid, ethylene, salicylic acid, and ROS while taking part
in elicitor-induced production of secondary metabolites [94, 126]. Although these
molecules operate through distinct defense signaling pathways, they are all known
to interact with NO in mediating plant secondary metabolite production [126].
The combination of elicitation with various biotic, abiotic stresses, and other signal
molecules implies NO as the keypoint in the signaling network leading to the
biosynthesis of some secondary metabolites [95]. Jasmonic acid induce NOS activity
and subsequent NO production leading to enhanced matrine accumulation in
Sophora flavescens suspension cells [99]. Similarly, NO-mediated accumulation of
fungal elicitor-induced puerarin production in P. thomsonii suspension cells occurs
through both SA-dependent or SA-independent signaling pathways [94, 95].
Although a direct link between methyl jasmonate and NO is yet to establish,
exogenous MeJA triggered a burst of NO during the accumulation of taxol from T.
chinensis cell cultures. Furthermore the suppression of NO by its inhibitors also
suppressed the MeJA-induced taxol production suggesting a central role of NO
in taxol accumulation [120]. Similarly, NO acts downstream to MeJA during the
accumulation of four tanshinone compounds in hairy root cultures of Salvia
miltiorrhiza [127]. However, SNP supplementation along with methyl jasmonate
leads to the marked decrease of the catharanthine production by repressing the
transcription of its biosynthetic genes, while methyl jasmonate supplementation
alone stimulated the transcription of catharanthine pathway genes suggesting an
antagonistic relation between NO and MeJA [127].
NO acts synergistically with reactive oxygen species to stimulate ethylene biosynthesis and stomatal closure in defense response to UV-B irradiation in maize
leave [92]. In another study, brassinolide pretreatment induced the production of NO
612
P. Santisree et al.
NO donor promoted volatile oil accumulation, while treatment with NO scavenger
inhibited the burst of salicylic acid and volatile oil accumulation induced by the
fungus. Likewise elicitation with another endophytic fungal Cunninghamella sp.
also induced the NO-mediated accumulation of atractylone, hinesol, β-eudesmol,
and atractylodin in suspension cells of A. lancea [104]. NO induced by cerebroside
elicitor from Fusarium was involved in the regulation of artemisinin production by
increasing the gene expression of 1-deoxy-D-xylulose 5-phosphate synthase and
hydroxybenzoate meta-geranyltransferase in A. annua hairy roots as well [102]. It
was reported that oligogalacturonic acid-induced NO accumulation could improve
the transcription of squalene synthase and squalene epoxidase, two early enzymes
for the synthesis of triterpenoid saponins in cell cultures of Panax ginseng [121].
Similarly, NO burst followed by the biosynthesis of torpinoid β-thujaplicin in
elicited Cupressus lusitanica cells which has strong antifungal, antiviral, and anticancer activities [126]. NO was found to reduce the transcription of genes in the
monoterpenoid indole alkaloids pathway and the octadecanoid-responsive
Catharanthus AP2/ERF domain transcription through the inhibition of type-I protein prenyltransferase gene, leading to a downregulation of the catharanthine biosynthesis [96].
NO may also interact with other signaling molecules integral of plant defense
system including jasmonic acid, ethylene, salicylic acid, and ROS while taking part
in elicitor-induced production of secondary metabolites [94, 126]. Although these
molecules operate through distinct defense signaling pathways, they are all known
to interact with NO in mediating plant secondary metabolite production [126].
The combination of elicitation with various biotic, abiotic stresses, and other signal
molecules implies NO as the keypoint in the signaling network leading to the
biosynthesis of some secondary metabolites [95]. Jasmonic acid induce NOS activity
and subsequent NO production leading to enhanced matrine accumulation in
Sophora flavescens suspension cells [99]. Similarly, NO-mediated accumulation of
fungal elicitor-induced puerarin production in P. thomsonii suspension cells occurs
through both SA-dependent or SA-independent signaling pathways [94, 95].
Although a direct link between methyl jasmonate and NO is yet to establish,
exogenous MeJA triggered a burst of NO during the accumulation of taxol from T.
chinensis cell cultures. Furthermore the suppression of NO by its inhibitors also
suppressed the MeJA-induced taxol production suggesting a central role of NO
in taxol accumulation [120]. Similarly, NO acts downstream to MeJA during the
accumulation of four tanshinone compounds in hairy root cultures of Salvia
miltiorrhiza [127]. However, SNP supplementation along with methyl jasmonate
leads to the marked decrease of the catharanthine production by repressing the
transcription of its biosynthetic genes, while methyl jasmonate supplementation
alone stimulated the transcription of catharanthine pathway genes suggesting an
antagonistic relation between NO and MeJA [127].
NO acts synergistically with reactive oxygen species to stimulate ethylene biosynthesis and stomatal closure in defense response to UV-B irradiation in maize
leave [92]. In another study, brassinolide pretreatment induced the production of NO
612
P. Santisree et al.