OLIGOGALACTURONIDES INHIBIT THE INDUCTION OF LATE BUT NOT OF EARLY AUXIN-RESPONSIVE GENES INVOLVED IN DIFFERENTIATION .

From recent studies in animals and plants the notion has emerged that disease resistance mechanisms and developmental processes may share regulatory signals .Oligogacturonides (OG), well known elicitors of plant defence responses, exhibit various regulatory effects on plant growth and differentiation. OGs are generally considered localised active signals and the effects induced by OGs in plant defence and development are considered to be receptor-mediated. The analysis of different responses produced by OGs suggests the existence of different pathways leading to the activation of defence responses or the regulation of developmental processes. In many of these latter effects OGs seem to act as antagonists to auxin. To investigate on the mechanism of the antagonism of OGs to auxin, we analysed the effect of different auxin-responsive promoters of genes likely to be involved in developmental and growth processes. Auxin-responsive genes are classified as early or late-responsive on the basis of the kinetics of their response to the hormone. In this work, we examined genes belonging to both classes. Analysis by GUS reporter gene shows that submicromolar concentrations of OGs with a DP of 9 to 18 inhibit the late auxin-regulated activation of the promoters of the genes pNt114 from tobacco, prolB and prolD from Agrobacterium rhizogenes in tobacco seedlings. In contrast, OG concentrations as high as 100 mg/ml, do not affect the early activation of pGm-GH3 from soybean, indicating that this promoter responds to auxin via an OG-insensitive signal transduction pathway. To confirm our results, we analysed by RNA gel blot the effect of OGs on two additional early auxin-responsive tobacco genes: Nt-gh3, a GH3 related gene and Nt-iaa 2.3/Nt-iaa 2.5, belonging to the Aux/IAA large multigene family. We demonstrate that, in addition to pGm-GH3 these early responsive genes are insensitive to OGs. Moreover histochemically analysis shows that the inhibitory effect exerted by OGs was not tissue-specific. The OG effect is not correlated with the auxin concentration necessary to activate the genes. These results taken toghether with a comparative analysis of promoter sequences suggest the possibility that OG-triggered transduction pathway(s) intersect(s) those induced by auxin far downstream of the perception event. A model of OG as auxin antagonist will be presented. The signalling element(s) at the intersection(s) between the OG and IAA transduction networks remains to be identified.