1.2.33
INVOLVEMENT OF ELICITOR-BINDING PROTEIN IN EXPRESSION OF DISEASE RESISTANCE IN SOYBEAN

N YAMAOKA1, Y TAKEUCHI1, S TERASAKA1, K MORI1, M KAKITANI2, N UMEMOTO2 and I ISHIDA2

2Cell Function and Structure, Division of Biological Sciences, Graduate School of Science, Hokkaido University, Sapporo 060, Japan; 2Central Laboratories for Key Technology, Kirin Brewery Co. Ltd, Fukuura, Kanazawa-ku, Yokohama 236, Japan

Background and objectives
The interaction between soybean (Glycine max) and beta-glucan elicitor (GE) from the phytopathogenic fungus Phytophthora megasperma f.sp. glycinea is one of the best characterized plant defence systems. The first event between soybean and the fungus is an attack of the fungal cell wall by soybean p 1,3-glucanase, resulting in the release of active GEs, which then initiate phytoalexin accumulation. It has been shown that specific binding sites to the GEs exist in the plasma membrane fraction of soybean. Recently, GE-binding protein (GEBP) has been purified from the soybean root membrane fraction and its cDNA sequence has been identified. In this study, the role of GEBP in disease resistance was evaluated by using a plant hormone, abscisic acid (ABA) as an inhibitor agent for GEBP expression.

Results and conclusions
More than 100 mM of ABA pretreatment was effective to suppress GEBP expression and phytoalexin accumlation by GE in soybean hypocotyls. ABA also inhibited GE-inducible accumlation of mRNA for phenylalanine ammonia lyase, which is involved in phytoalexin biosynthesis. Furthermore, hyphal growth of an incompatible race of P. megasperma f.sp. glycinea increased in ABA pre-treated soybean hypocotyls. These results suggest that decrease in expression level of GEBP may result in inhibition of elicitor-signal transmission leading to induction of a defence response, and GEBP may play an important role in expression of soybean disease resistance.

References
1. Umemoto N, Kakitani M, Iwamatsu A, et al., 1997. Proceedings of the National Academy of Sciences, USA 94, 1029-1034.