## 1 The Concept of Phytoalexins  
The concept of phytoalexins, that is antimicrobial substances of low molecular weight produced by plants in response to infection or stress, was proposed in 1940 by [PERSON] and [PERSON] [1] in the study of the interaction between potato and _Phytoophthora infestans_. Briefly, the inhibition of the development of a race of \(P\). _infestans_ which normally develops profusely on potato tubers following infection of the potato tubers with another race of \(P\). _infestans_ able to initiate hypersensitive reaction (HR), was caused by a \"principle\" produced by the hypersensitivity-reacting plant cells. The principle was named a phytoalexin. The term phytoplankton was derived from Greek to mean \"warding-off agents in plants\" and the proposal of this elegant concept was made after deliberating two important phenomena in plant pathology. The first one is the active response of the plant cell to attempted infection; the second one is the acquisition of resistance by plants after exposure to microorganisms [2]. A fundamental feature of this definition is that it restricts phytoalexins to compounds which are produced from remote precursors, through _de novo_ synthesis of enzymes. At the time they have been discovered, phytoalexins were, therefore, clearly distinguished from other antimicrobial substances which are pre-formed or arise directly from inactive precursors [3]. As a corollary, the fact that these compounds constitute a defense response of plants to biotic and abiotic stresses, makes the regulatory networks involved in their induction extremely complex. For instance, studies on the signaling pathways controlling the induction of camalexin, the major phytoalexin from _Arabidopsis_, particularly underline the complexity of these regulatory mechanisms, which in turn depend on the infecting pathogen [4]. From reports evaluating the response of _Arabidopsis_-jasmonic acid (JA) mutants to _Alternaria brasscicola_ it ensued that synthesis of this phytoplankton was not JA-dependent [5, 6]. Conversely, JA has been found to form part of the regulatory pathways for camalexin biosynthesis in the response of that plant to _Botrytis cinerea_[7]. In fact, absence of functional jasmonate signaling in _Arabidopsis_ mutants resulted in dramatic differences in phytoalexin accumulation upon infection by _B. cinerea_. Other results showed that the regulation of camalexin production can be controlled by salicylic acid (SA)-independent [8, 9] or SA-dependent [10] signaling pathways. Camalexin production was also found to be decreased in response to bacterial or fungal infection in _Arabidopsis_ mutants impaired in ethylene signaling [5, 11]. Suppression of auxin signaling in _Arabidopsis_ re-directed secondary metabolism towards glucosinolates and away from camalexin [12] (see section 4). Recent works have reported a regulation of camalexin biosynthesis involving two Mitogen-Activated Protein Kinases (MAPKs), inducing in turn the responses further downstream, especially camalexin accumulation [13] (see section 5). The two transcriptions factors WRKY40 and WRKY18 were also found to be involved in the regulation of some enzymes of the camalexin pathway, namely regulation of the cytochrome P450 monoxoygenase 71A13 catalyzing transformation of indole acetaldoxime to indole-3-acetonitrile on the route to camalexin [14]. Based on this example, it thus appears thatregulatory pathways for phytoolexin induction are complex. Modulation of phytoolexin biosynthesis in engineered plants for disease resistance typically reflects this complexity. Phytoolexins form part of the defense mechanisms of plants against phytopathogenic microorganisms. These are antibacterial, antifungal and antiviral compounds showing phytotoxic activities as well. It is now clear that phytoolexins exhibit toxicity across much of the biological spectrum, prokaryotic and eukaryotic, and that their activities are by no means confined to phytopathogenic fungi though considerable work has been done on plant/fungus interactions [15].