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FARHA-REHMAN ET AL.
pathway for activating plant defense genes against attacking herbivores and
pathogens is mediated by a lipid based signal transduction cascade. In this pathway,
linolenic acid (18:3) is liberated from cell membranes and is converted to
cyclopentanones involved in transcriptional regulation of plant defense genes
(Conconi et al., 1996).
A wide range of genes in plants are activated on herbivore attacks, and their
activation is strongly correlated with the mode of herbivores feeding and degree of
tissue damage at the feeding site (Walling, 2000). Phloem feeding whiteflies and
aphids producing little injury to plant foliage were perceived as pathogens and
activate the salicylic acid (SA)-dependent and JA ethylene-dependent signalling
pathways. Volatiles blends provided specific cues to attract specialist parasites and
predators to attack infesting herbivores (Walling, 2000).
Herbivory on lima bean leaves induced volatiles elicitor defence genes
(Arimura et al., 2000). In uninfested lima bean leaves, five separate sets of defense
genes were activated on exposure to volatiles from co-specific leaves infested by
Tetranychus urticae. All these genes were not activated when uninfested leaves were
exposed to volatiles from artificially wounded leaves (Arimura et al., 2000). The
expression pattern of these genes was similar to that produced on exposure to JA. At
least three terpenoids of the released volatiles were responsible for the gene
activation, which were released in response to herbivory but not on artificial
wounding. Expression of these genes required calcium influx and protein
phosphorylation/dephosphorylation (Arimura et al., 2000).
The herbivore induced volatiles in Arabidopsis thaliana attracted the parasitoid
Cotesia robecula (Van Poecke, Posthumus, & Dicke, 2001). The A. thaliana plants
infested by Pieris rapae emitted volatiles from several major biosynthetic pathways,
including terpenoids and green leaf volatiles. Haq et al. (2004) focused on the utility of
the protein proteinase inhibitor genes in combating insects, pests, and pathogen as
natural and engineered phytoprotection. Devoto et al. (2005) found COII as a key
regulator of genes involved in wound. The methyl jasmonate induced secondary
metabolism, defence and hormone interactions. COII expressed approximately 84% of
212 genes induced by JA, and approximately 44% of 153 genes induced by wounding.
COII displayed a pivotal role in wound and JA signalling (Devoto et al., 2005). The
volatile emission on green leaf wounding induced the release of acetylated derivatives
and a terpenoid in maize, and these compounds in turn induced JA production in intact
plants (Yan & Wang, 2006). The wound-induced green leaf volatiles (GLVs) caused
the release of acetylated derivatives and a terpenoid, (E)-4,8-dimethylnona-1, 3, 3-
triene (DMNT) in intact maize, which may be a type of plant-plant interaction
mediated by airborne GLVs (Yan & Wang, 2006).
Karban and Niiho (1995) worked on plant “memory” to induce resistance and
susceptibility to herbivory. Many plants have been found to be highly induced by
repeated herbivory, than by a single herbivore bout. The frequency and magnitude of
damage were confounded and thus it was not clear if a biochemical “memory” was
involved or overall damage amplified the induced response (Karban & Niiho, 1995). In
this experiment, the cotton plant attacked by spider mites and mechanical damage of
cotyledon induced resistance, but damage of apical buds induced susceptibility, due to
differentially affected hormonal regulation in both tissue types (Karban & Niiho, 1995).