82 Produce Degradation: Reaction Pathways and their Prevention
tissues. Nicotinamide and its metabolites appear to play a role in DNA hypometh-
ylation, as a link between various types of stressors and the induction of plant
defensive metabolism.^22
Wounding induces expression of genes encoding defense-related proteins
involved in wound healing. Plants react to mechanical injury produced by abiotic
or biotic agents by activating a set of responses that include, in most cases, the
transcriptional activation of wound responsive (WR) genes. Some of these genes are
expressed in the vicinity of the wound site, while others are also systematically
activated in the undamaged parts of the plant tissue. Some of them may have a
defensive role against organisms that attack the plant tissue and prevent subsequent
pathogen invasion, while others may work to facilitate wound healing. Some of the
induced proteins are enzymes of phenolic metabolism, such as phenylalanine ammo-
nia-lyase (PAL), whose increased activity leads to the accumulation of phenolic
compounds (e.g., chlorogenic acid, dicaffeoyl tartaric acid, and isochlorogenic acid)
and tissue browning. Wounding of iceberg lettuce leaves increases PAL activity 6-
to 12-fold over 24 h at 10°C and leads to a threefold increase in the total phenolic
content within 3 days. There may be a hierarchical order to the plant’s response to
different abiotic stresses.^23 Plants respond differentially to wounding and pathogens
using distinct signaling pathways; wound signals are transmitted to jasmonic acid
(JA), which induces basic pathogenesis-related (PR) proteins, whereas pathogenic
signals cause, in addition to JA, accumulation of salicylic acid (SA), which stimulates
production of acidic PR proteins.^24
Jasmonic acid has been considered to be a key signal molecule in this pathway.
Allene oxide synthase (AOS; hydroperoxide dehydratase; EC 4.2.1.92) catalyzes the
first step in the biosynthesis of jasmonic acid from lipoxygenase-derived hydroper-
oxides of free fatty acids. The addition of silver thiosulfate, an ethylene action
inhibitor, prevented the wound-induced expression of both AOS and proteinase
inhibitor II (PIN II). Products of hydroperoxide lyase affected neither AOS nor PIN
II but induced expression of prosystemin.^25 Systemin, ABA, ethylene, and electrical
current have been suggested to function by transmitting the wound signal to JA.^26
Ethylene treatment may, however, inhibit the methyl-JA-induced expression. The
defensive gene expression induced by signal transduction through the octadecanoid
pathway is suppressed by stress-induced ethylene that is produced as a consequence
of wounding.^27 Ethylene also inhibits its own biosynthesis by decreasing 1-amino-
cyclopropane-1-carboxylate (ACC) synthase transcript levels via a negative feedback
loop.^28 ACC is the product of ACC synthase and the immediate precursor to ethylene.
Different jasmonic acid-dependent and -independent wound signal transduction
pathways have been identified recently and partially characterized. Components of
these signalling pathways are mostly similar to those implicated in other signalling
cascades in eukaryotes and include reversible protein phosphorylation steps, cal-
cium/calmodulin-regulated events, and production of active oxygen species. Indeed,
some of these components involved in transducing wound signals also function in
signalling other plant defence responses, suggesting that cross-talk events may
regulate temporal and spatial activation of different defences.^29 Other compounds,
including the oligopeptide systemin, oligosaccharides, and other phytohormones
such as ABA have also been proposed to play a role in wound signaling.^29