**4. Conclusion**

380 Lipid Metabolism

between 48 and 96hai.

nsLTPs mRNAs accumulation.

**Figure 8.** *ltp* gene expression in wheat leaves treated with SA

Moreover, LTPs are known to be differentially expressed during a pathogenic interaction because they are potentially good ligands to oleic C18:1, linoleic C18:2 and eicosadienoic acids C20:2 [110]. Among 28 identified wheat nsLTP, eight nsLTP expressed in yeast exhibited lipid binding activity [111]. These proteins could be involved in the intracellular

**3.6.** *ltp* **gene expression is induced by SA infiltration** 

The effect of SA on the expression of a lipid transfer protein-encoding gene *ltp* was also conducted according to the same time-course experiment (figure 8). SA induced a biphasic *ltp* expression pattern: a 1.7-fold increase at 9hai followed by an average of 4.6-fold increase

The LTPs extracellular distribution in the exposed surfaces in vascular tissue systems, high abundance and corresponding genes expression in response to infection by pathogens suggest that they are active plant-defense proteins [106]. A combined expression of chitinase and LTP-encoding genes in transgenic carrot plants enhances resistance to *Botrytis sp.* and *Alternaria sp.* [107]. A high global expression of an *ltp* gene in resistant wheat to *Tilletia tritici* was identified [108]. The nonspecific nsLTP-encoding gene expression profile was evaluated in grape cells suspension in response to various defenserealted signal molecules [109]. A rapid and strong accumulation of nsLTPs mRNAs was recorded upon treatment with ergosterol (5h after treatment with hybridation signal more than 300X A.U.) whereas JA, cholesterol and sitosterol promoted an accumulation but to a lesser extent (hybridation signal between 100 and 200X). However, SA had no effect on

The present chapter provides evidences for the effect of resistance inducers on wheat lipid metabolism and presents the strategy we used in order to characterize their mode of action at different levels: total FA content and relative proportion, PA, PE and DAG contents, expression of genes such as PLC and LTP-encoding ones. Lipid metabolism is therefore a marker of induced resistance in wheat. To our knowledge, such findings have never been presented before on *Triticum aestivum*.

Salicylic acid is very likely to induce the formation of PA through the activation of phospholipases C and/or D pathways: induction of *PLC* gene expression, together with DAG accumulation suggests that the PLC pathway is enhanced and leads to PA production. On the other hand, reduction of PE content suggests that PLD pathway is triggered upon SA infiltration in order to ensure PA synthesis. *lox* gene expression up-regulation and corresponding enzymatic activity, along with the decrease of linolenic acid content, suggests that SA modulates lipid enzymatic peroxidation. Moreover, the expression of *ltp* gene was induced by SA, showing the involvement of the corresponding protein in the lipid signaling metabolism.

The tested resistance inducers had some similarities in their mode of action, relatively to total FAs profiles. Trehalose and Milsana® seem to share similar modes of action via the increase of C12:0 and decrease of C20:2 contents. Iodus® exhibited the largest effects on FAs profiles, inducing increases in C12:0 and C18:1 and decreases in C20:2. HSA, however, was the only resistance inducer that modulated positively the content of C18:2.

Future investigations have to be extended to other genes expression and corresponding enzymatic activities acting downstream of lipoxygenase in order to figure out whether the LOX-derived hydroperoxides are metabolized during the JA synthesis. Furthermore, a global approach using microarrays based on wheat cDNA chips would be a useful tool for increasing our knowledge of the plant lipidome in our wheat-powdery pathosystem.
