2.8.3. biosynthesis of the JA precursor linolenic

2.8.3. Jasmonic acid

The role of
Jasmonic acid (JA) signalling in defence was shown using Arabidopsis mutants
affected in the biosynthesis or perception of JA. A JA-response mutant, coi1,
displaying susceptibility to the nectrophic fungi Alternaria brassicicola and
Botrytis cinerea (Thomma et al., 1998), was used to confirm the
role of JA in defence. Two mutants which were deficient in the biosynthesis of
the JA precursor linolenic acid, jar1 (Staswick et al., 1992) and
a fad3 fad7 fad8 triple mutant from Arabidopsis, also showed
susceptibility to normally non-pathogenic soil-borne Pythium spp,
indicating that JA plays a role in non-host resistance against pathogens. This
also shows that JA-dependent defences contribute to basic resistance against
different microbial pathogens and confirms that JA is important in the basic
resistance against herbivorous insects (Staswick et al., 1998; Vijayan et
al., 1998; Pieterse et al., 2001).

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2.8.4. Ethylene

Ethylene is a
gaseous plant hormone that plays a role in various developmental processes
(Zhou and Thornburg, 1999). It is synthesized from S-adenosyl-L-methionine
via 1-aminocyclopropane-1-carboxylic acid (ACC) and plays an important role in
various plant disease resistance pathways (Zhou and Thornburg, 1999; Guo and
Ecker, 2004). Plants deficient in Ethylene signalling show either increased
susceptibility or increased resistance (Wang et al., 2002). Ethylene
seems to suppress symptom development during necrotrophic pathogen infection,
but enhances the cell death caused by a different type of pathogen infection.
An example of this is soybean mutants with reduced Ethylene sensitivity that
produce less severe chlorotic symptoms when challenged with the virulent Pseudomonas
syringae pv glycinea and Phytophthora sojae strains (Hoffman et
al., 1999), whereas virulent strains of the fungi Septoria glycines and
Rhizoctonia solani cause more severe symptoms (Hoffman et al.,


2.8.5. Pathogenesis-related

Both pathogen-
and Salicylic acid (SA) induced resistance are associated with the induced
expression of several families of Pathogenesis-Related
(PR) genes during the HR. The induction of PR gene expression is
regularly linked to necrotizing infections giving rise to SAR, and has been
used as a marker of the induced defensive state (Ward et al., 1991a;
Uknes et al., 1992). PR proteins play a major role in the defence
response in many plants under stress and are detected in plants after exposure
to insects (Bronner et al., 1991; van der Westhuizen and Pretorius,
1995; Broderick et al., 1997; van der Westhuizen et al., 1998).
The accumulation of PR proteins during the onset and maintenance of SAR is
thought to be responsible for the enhanced resistance of the uninfected plant
tissues so that they are referred to as SAR proteins. The PR4 gene in
wheat is an example of a gene that is expressed when the plant is exposed to
chemical activators of SAR and wounding (Bertini et al., 2003). Two
other important PR proteins are ?-1,3-glucanases and chitinases. During plant
defence, ?-1,3-glucanases and chitinases are believed to respond by degrading
hyphal walls of the pathogen (Leah et al., 1991; Jach et al.,
1995; Lawrence et al., 1996; White et al., 1996). ?-1,3-glucanases

form part of the PR2 protein family that is able to catalyse endo-type
hydrolytic cleavage of the 1,3-?-D-glucosidic linkages in ?-1,3-glucans
(Leubner-Metzger and Meins, 1999). It is suggested to play a role in the
response of plants to pathogen attack (Côte et al., 1991; Ward et al.,
1991a) and other stimuli (Memelink et al., 1990). ?-1,3-glucanases are
divided into four classes. Class I is produced as a pre-protein with an
N-terminal hydrophobic signal peptide which is co-translationally removed and a
C-terminal extention that is N-glycosylated at a single site. The proteins in
this class are localized in the cell vacuole. Class II, III and IV are acidic
proteins lacking the C-terminal extension present in the class I enzymes and
are secreted into the extracellular space (van Loon and van Strien, 1999). Chitinases

Plant chitinases
are suggested to be involved in plant disease resistance during pathogen
infection (Cheng et al., 2002). Chitinases catalyses the hydrolysis of
chitin which is a linear polymer of ?-1,4-linked N-acetylglucosamine
residues (Khan and Shih, 2004). Chitinases have been found to be activated by
fungal infection and plant activators such as INA and BTH which induce SAR
(Busam et al., 1997).


2.8.6. Programmed cell death

Programmed cell
death is an active process occurring in response to environmental stresses and
pathogen infection (Jabs and Slusarenko, 2000; Greenberg and Yao, 2004).
Programmed cell death involves chromatin aggregation, cytoplasmic and nuclear
condensation and fragmentation of the cytoplasm and nucleus into membrane-bound
vesicles (Jabs and Slusarenko, 2000). Membrane damage is the first sign of
programmed cell death. Cells that are killed usually autofluoresce and become
dark brown due to the accumulation and oxidation of phenolic compounds (Heath,
2000). The role of programmed cell death during pathogenesis is to limit the
spread of disease after the induction of HR at the site of infection
(Greenberg, 1996; Lam et al., 2001; Greenberg and Yao, 2004). There are
two different mechanisms involved in cell death occurring during the compatible
and incompatible interactions respectively (Greenberg, 1997). The mechanism by
which cell death occurs in susceptible plants is not fully understood, but it
is thought that a toxin produced by the pathogen may directly kill the plant
cells. In the resistant interaction, HR is induced and rapid cell death occurs
(Greenberg, 1997).