## 4 Modulation of Phytoalexin Accumulation through Engineering of Plant Hormones  
The essential role played by phytohormones in the induction of plant defense responses has been reviewed elsewhere [101; 102; 103; 104; 105; 106; 107; 108; 109]. Defense responses against biotrophs and necrootrophs are classically based on two antagonistic pathways, SA signaling controlling defense against biotrophs, JA/ethylene signaling controlling defense against necrootrophs. Some aspects of the involvement of SA, JA/ethylene in phytoalexin induction have been discussed in the particular case of camalexin (see section 1). There are also some examples of phytoalexin accumulation being up- or downregulated by overexpression of other signaling molecules such as auxins, abscisic acid, cytokins and gibberellins. Auxin homeostasis is considered as one of the components participating in the regulation of plant defense responses [110; 111]. In many instances, auxins appear to negatively regulate plant defense mechanisms. In the case of plant/virus interactions, there are some examples relating auxin depletion and pathogen resistance [112; 113; 114]. Overexpression of _OsGH3.8_, a member of the _GH3_ gene family which encodes an indole-3-acetic acid-amido synthase in rice, acts as an activator of disease resistance by transient and cell-specific suppression of auxin signaling [115]. Constitutive overexpression of _OsGH3.1_ was shown to reduce auxin content and to enhance defense responses and resistance to _Magnaporthe grisae_ in rice [111]. Thirty four defense genes were up- and down-regulated in the transgenic rice plants overexpressing _OsGH3.1_ though no information were provided concerning phytoalexin gene induction in this case. [PERSON] and colleagues have shown recently that the increased susceptibility to biotrophic pathogens and re-direction of phytoalexin metabolism observed in _Arabidopsis_ plants overexpressing the _AFB1_ gene (which encodes an auxin receptor and whose mRNA is partially resistant to a targeting auxin receptor- microRNA), were probably due to the negative effect of auxin on SA signaling [12]. Conversely, targeting of the auxin receptor mRNAs by overexpression of the microRNA miR393 resulted in direct suppression of auxin signaling and stabilization of inactive AUX/IAA-ARF, which negatively regulate auxin signaling through binding and inactivation of auxin response factors. Suppression of auxin signaling allowed the plant to mount a full SA response and to re-direct secondary metabolism towards the more fungitoxic phytoanticipins, glucosinolates [116] and away from the less fungitoxic phytoalexin camalexin. The plant hormone abscisic acid (ABA) regulates the adaptive response of plants to environmental stresses such as drought, salinity, and chilling as well as biotic stresses _via_ diverse physiological and developmental processes. As for auxins, it seems that ABA depressed fungal, bacterial and viral resistances of plants by negatively regulating genes involved in plant defense mechanisms though there are some reports of stress-induced elevated ABA concentrations being associated with decreased susceptibility to fungal pathogens, for instance in tomato challenged with _Phyophthora parasitica_[117]. Loss-of-function mutations in the ABA pathway led to ABA deficiencies and increase in disease resistance in tomato to, respectively, the necrotrophic fungus _B. cinerea_[118] and the pathogenic bacterium _Erwinia chrysanthemi_[119]. Exogenous applications of ABA made tobacco plants more susceptible to Tobacco Mosaic Virus (TMV) [120] and led to the down-regulation of genes encoding PR protein \(\beta\)-1,3-glucanase isoforms in tobacco cell cultures [121]. ABA was also involved in the regulation of phytoalexins. The synthesis of the bean (_Phaseolus vulgaris_) phytoalexin kievitone was downregulated by ABA [122]. ABA reduced glyceollin production in soybean as a response to _Phytophthora megasperma_[123] or _P. sojae_[124], as well.