RHIZOBIUM NOD FACTOR SIGNALING - EVIDENCE FOR A G-PROTEIN-MEDIATED TRANSDUCTION MECHANISM

Rhizobium nodulation (Nod) factors are lipochitooligosaccharide signal s that elicit key symbiotic developmental responses in the host legume root. In this study, we have investigated Nod factor signal transduct ion in the Medicago root epidermis by using a pharmacological approach in conjunction with transgenic plants expressing the Nod factor-respo nsive reporter construct pMtENOD12-GUS. Evidence for the participation of heterotrimeric G proteins in Nod factor signaling has come from th ree complementary observations: (1) the amphiphilic peptides mastopara n and Mas7, known G protein agonists, are able to mimic Nod factor-ind uced epidermal MtENOD12 expression; (2) growth of plants in nodulation -inhibiting conditions (10 mM NH4NO3) leads to a dramatic reduction in both Nod factor-and mastoparan-elicited gene expression; and (3) bact erial pertussis toxin, a well-characterized G protein antagonist, bloc ks the activities of both the Nod factor and mastoparan. In addition, we have found that antagonists that interfere with phospholipase C act ivity (neomycin and U73122) and Ca2+ influx/release (EGTA, La3+, and r uthenium red) block Nod factor/mastoparan activity. Taken together, th ese results are consistent with a Nod factor signal transduction mecha nism involving G protein mediation coupled to the activation of both p hosphoinositide and Ca2+ second messenger pathways.