Involvement of lipoxygenase in resistance of wheat against the Russian wheat aphid

English: The upstream role of lipoxygenase (linoleate: oxygen reductase, E.C. 1.13.11.12) in the induced defence response against the Russian wheat aphid (Diuraphis noxia) was studied in resistant wheat (Triticum aestivum L.) cultivars Tugela-DN (Dn1), Tugela (Dn2) and Tugela (Dn5) and the near isogenie susceptible cultivar, Tugela. The RWA induced LOX was partially characterised. The pH for optimum LOX activity was 5.6 and it had no requirement for cofactors such as K+, Mg2+ or Ca2- The enzyme also had a high affinity for linoleic acid, with a Km-value of -5.8 x 10-4M. LOX activity was selectively induced in infested resistant Tugela cultivars containing the (Dn1), (Dn2) and, to a lesser extent, (Dn5) resistant genes. The differential induction of LOX activity corresponded with the induction of the hypersensitive response during the resistance response of Tugela-DN against the RWA. The incorporated resistant gene affected the level of induced LOX activity, which roughly corresponded with the cultivars' levels of resistance. Localised RW A infestation led to a systemic increase in LOX activity. All indications were that the induced LOX activity was involved in the resistance response in wheat against the RWA. Inhibitory studies were performed with LOX inhibitors, piroxicam, salicylhydroxamic acid and n-propyl gallate, to shed light on the possible upstream role of LOX. Piroxicam was the most suitable inhibitor due to the fact that it only inhibited LOX activity in vitro. Inhibition of LOX activity in vivo by piroxicam, led to the inhibition of 'downstream' defence responses such as peroxidase and β-l ,3-glucanase activities. The selective increase in LOX activity did not correlate with a selective increase in jasmonic acid concentrations. The effect of intercellular injected JA on LOX, peroxidase and β-1 ,3- glucanase activities, indicated that jasmonic acid was not the primary product of the RWA induced LOX activity and that it was not the signal molecule in the RWA /wheat resistance response. The products of the RWA induced LOXs appeared to be derived from the 9-hydroperoxide derivative pathway, rather than the 13- hydroperoxide derivative (jasrnonic acid precursor) pathway. Neither was abscicic acid a product of the selective increased LOX activity, nor playing a role in the RWA resistance response in wheat. Other studies in our laboratory showed that salicylic acid is probably the signal molecule, activating defence genes after elicitation. It is evident that the RWA resistance response corresponded with that of pathogenesis, and that each defence response follows its own distinctive defence cascade.