Conversely, lack of recognition (a compatible reaction) of such a product by the plant is characterized by
pathogen virulence and results in infection of the plant by the pathogen and subsequent plant disease.
A plant has both constitutive and inducible defenses. A type of inducible biotic stress defense re-
sponse is systemic acquired resistance (SAR), an increase in resistance throughout the entire plant to at-
tack by a broad spectrum of pathogens, typically effected over a period of days to a week following ini-
tial pathogen attack. The region immediately under attack, however, achieves local acquired resistance
(LAR), which may be separate from SAR. Among the first symptoms of an incompatible interaction be-
tween a plant and a pathogen is the hypersensitive response (HR), a component of both LAR and SAR.
The HR is a localized, rapid necrosis of the tissue at the infection site, in part due to a phenomenon re-
ferred to as an oxidative burst [2]. The oxidative burst produces reactive oxygen species or intermediates
(ROS, ROI) that are apparently necessary but not sufficient for cell death to occur. Such ROS also have
antimicrobial effects, although their contribution to defense is still a matter of conjecture [2]. Rather than
being a symptom of infection and resulting from trauma, sufficient data have been collected to suggest
strongly that the HR is an example of programmed cell death (PCD), which is under coordinated, genetic
control [3]. It should also be noted that colonization of roots by rhizogenic bacteria has also been shown
in some species to give rise to a heightened resistance to foliar pathogens. This type of SAR has also been
termed induced systemic resistance (ISR) [4].
The oxidative burst stimulates the synthesis of salicylic acid (SA), which is associated with SAR and
appears to be largely responsible for transmitting the induction of defense responses throughout the plant
[2]. SAR is manifested by changes in protein synthesis, de novo synthesis, and increased synthesis of spe-
cific defense proteins or proteins involved in metabolic biosynthetic pathways. These changes are gener-
ally similar for fungal, bacterial, and viral pathogens, with many proteins or biosynthetic pathways in-
duced in common. Some of the proteins and enzymes that accumulate during LAR and SAR are involved
in lignification of the cell wall. Lignified cell walls are highly resistant to cell wall–degrading enzymes
produced by many invading pathogens and therefore prevent or limit infection. Another general response
is the production of a class of nonproteinaceous compounds called phytoalexins, which appear to act as
antimicrobial compounds. The compounds are structurally complex, with chemical derivation paralleling
and specific to the species in which they are synthesized. The following sections are a brief summary of
the better known biotic defense responses.
B. Cell Wall Modifications
Cell wall–modifying proteins encompass two groups, proteins that alter the cell matrix and enzymes in-
volved in lignification. The cell wall matrix proteins are typically hydroxyproline-rich glycoproteins (ex-
tensins) or glycine rich. They appear to function by providing a framework for the cross-linking of car-
bohydrate (pectin, cellulose) or polyphenolic (lignin, suberin) moieties [5,6]. These proteins are inducible
by ethylene (wounding), fungal elicitors, or viral infection [6]. The cell wall–modifying enzymes are
mostly peroxidases, which catalyze the suberization and lignification of cell walls [6]. They are involved
in the normal synthesis of cell walls but are also inducible by fungal elicitors [5] and may act in concert
with enzymes involved in the biosynthesis of phenolic compounds [6]. The thickening of the cell walls
then serves to wall off the pathogen and acts as a deterrent to further invasion.
Phenolic compounds utilized in the modification of cell walls have the same biosynthetic origin as the
isoflavonoid phytoalexins: the phenylpropanoid pathway. This pathway is, in turn, a branch of the shikimic
acid pathway, responsible for the synthesis of aromatic amino acids [7]. The precursor in the phenyl-
propanoid pathway, phenylalanine, is converted to 4-coumaryl-coenzyme A (CoA) by the involvement of
phenylalanine-ammonia lyase (PAL), cinnamate-4-hydroxylase (C4H), and 4-coumaryl-CoA ligase
(4CL) [7]. These enzymes, present during normal metabolism, increase dramatically and rapidly upon ex-
posure to pathogens. This has been shown to occur at the level of both gene transcription and translation
[6]. 4-Coumaryl-CoA serves as a branch point for the synthesis of lignin as well as of (iso)flavonoids. Hy-
droxylation of 4-coumaryl-CoA produces caffeic acid, which is successively modified to make ferulic and
sinapic acids, as well as coniferyl alcohol [7]. Peroxidase-catalyzed polymerization of the alcohols corre-
sponding to ferulic and sinapic acids, as well as coniferyl alcohol, gives rise to lignin [6,8]. Cinnamyl al-
cohol dehydrogenase is integral to this process and has been reported to be induced by fungal elicitors in
several systems [9–12] and by ozone in spruce [13]. Inducibility by ozone indicates that the enzyme su-
peroxide dismutase (SOD) may also be involved in this process. One of the products of SOD is H 2 O 2 , a
658 ARTLIP AND WISNIEWSKI