elucidation of its role in the production of such pharmaceutically significant
secondary metabolites is crucial for improving the large-scale commercial
production.
4.1
NO-Mediated Elicitation of Secondary Metabolites Under
Abiotic Stress
Several studies (mentioned in above sections) have demonstrated the alteration in
the secondary metabolite profile under abiotic stress in plants. NO can also increase
production of secondary metabolites and activate plant protection systems even
under stress conditions [94, 114]. Several abiotic and biotic elicitors can induce
NO-mediated regulation of the biosynthetic pathways of metabolites that can consequently alter growth and development in plants [95]. However, very little is known
on NO signaling in the biosynthesis of plant secondary metabolites under stress.
Given the production of NO in plants in response to abiotic and biotic stresses [106,
107, 111, 123 ], it can be presumed that NO may have the most possible and
prominent role in inducing secondary metabolites in response to stress. Hence, the
elicitor or stress-induced NO production is essential for triggering the biosynthesis
of critical secondary metabolites in plants [95]. Cu
2+ stress could induce NO
production and subsequent proline accumulation in Chlamydomonas reinhardtii
and in roots of P. ginseng [115]. In another study, ultrasound treatment for 2 min
resulted in a rapid and dose-dependent NO production in T. yunnanensis cell cultures
which in turn stimulated the production of taxol and baccatin III [120].
An interesting study suggested that NO treatment created a strong demand
for cysteine synthesis as a way to reduce oxidative stress. Cysteine synthesis is
one of the rate-limiting steps for the formation of glutathione which is very crucial
component in cellular redox responses. In agreement with that, active synthesis of
amino acids specifically α-ketoglutarate-derived amino acids of the glutamate family
was evident in response to NO treatment [94]. It is known from earlier reports that
the metabolism of γ-aminobutyrate (GABA) is crucial plants exposed to low oxygen
or high light condition. Exposure of plants to NO showed a moderate increase in
the levels of GABA and 2-aminobutyrate and the significant increase for γhydroxybutyrate.
A recent metabolomic data suggested a significant increase in metabolites
involved in purine and pyrimidine metabolism by 6 h after NO treatment. There
was a significant increase in the levels of allantoin, guanine, urate, cytidine, cytosine2
0 ,3
0 -cyclic monophosphate, pseudouridine, uridine, and uracil by NO. On the other
hand, NO treatment induced chlorophyll degradation as evident by an increment in
the levels of pheophorbide, a breakdown intermediate product of chlorophyll in
plants [19, 124].
NO is one of those key signaling molecules in elicitor-induced secondary metabolite biosynthesis in plant cells. Although pharmacological experiments with NO
donor and scavenger showed that the occurrence of NO contributes to strengthening
the transcription of genes encoding key enzymes involved in the biosynthesis of
610
P. Santisree et al.
secondary metabolites is crucial for improving the large-scale commercial
production.
4.1
NO-Mediated Elicitation of Secondary Metabolites Under
Abiotic Stress
Several studies (mentioned in above sections) have demonstrated the alteration in
the secondary metabolite profile under abiotic stress in plants. NO can also increase
production of secondary metabolites and activate plant protection systems even
under stress conditions [94, 114]. Several abiotic and biotic elicitors can induce
NO-mediated regulation of the biosynthetic pathways of metabolites that can consequently alter growth and development in plants [95]. However, very little is known
on NO signaling in the biosynthesis of plant secondary metabolites under stress.
Given the production of NO in plants in response to abiotic and biotic stresses [106,
107, 111, 123 ], it can be presumed that NO may have the most possible and
prominent role in inducing secondary metabolites in response to stress. Hence, the
elicitor or stress-induced NO production is essential for triggering the biosynthesis
of critical secondary metabolites in plants [95]. Cu
2+ stress could induce NO
production and subsequent proline accumulation in Chlamydomonas reinhardtii
and in roots of P. ginseng [115]. In another study, ultrasound treatment for 2 min
resulted in a rapid and dose-dependent NO production in T. yunnanensis cell cultures
which in turn stimulated the production of taxol and baccatin III [120].
An interesting study suggested that NO treatment created a strong demand
for cysteine synthesis as a way to reduce oxidative stress. Cysteine synthesis is
one of the rate-limiting steps for the formation of glutathione which is very crucial
component in cellular redox responses. In agreement with that, active synthesis of
amino acids specifically α-ketoglutarate-derived amino acids of the glutamate family
was evident in response to NO treatment [94]. It is known from earlier reports that
the metabolism of γ-aminobutyrate (GABA) is crucial plants exposed to low oxygen
or high light condition. Exposure of plants to NO showed a moderate increase in
the levels of GABA and 2-aminobutyrate and the significant increase for γhydroxybutyrate.
A recent metabolomic data suggested a significant increase in metabolites
involved in purine and pyrimidine metabolism by 6 h after NO treatment. There
was a significant increase in the levels of allantoin, guanine, urate, cytidine, cytosine2
0 ,3
0 -cyclic monophosphate, pseudouridine, uridine, and uracil by NO. On the other
hand, NO treatment induced chlorophyll degradation as evident by an increment in
the levels of pheophorbide, a breakdown intermediate product of chlorophyll in
plants [19, 124].
NO is one of those key signaling molecules in elicitor-induced secondary metabolite biosynthesis in plant cells. Although pharmacological experiments with NO
donor and scavenger showed that the occurrence of NO contributes to strengthening
the transcription of genes encoding key enzymes involved in the biosynthesis of
610
P. Santisree et al.