REGULATION OF SWEET-POTATO GROWTH AND DIFFERENTIATION BY GLUTAMATE-DEHYDROGENASE

The function of glutamate dehydrogenase was studied in cultured sweetp otato (Ipomoea batatas) nodal explants. The glutamate dehydrogenase wa s fractionated to charge isomers. Supplementation of the growth medium with either naphthaleneacetic acid or benzyladenine in the presence o f 20 mM NH4NO3 induced normal growth (type 1 sweetpotato). The basic a nd acidic charge isomers of glutamate dehydrogenase were not suppresse d. Combined supplementation with 70 mM NH4+ and either 1 mg . L-1 benz yladenine or 0.1 mg . L-1 naphthaleneacetic acid caused growth retarda tion (type 2 sweetpotato) and the suppression of the basic charge isom ers. Combined supplementation with 45 mM NH4+ and either 1 mg . L-1 be nzyladenine or 0.1 mg . L-1 naphthaleneacetic acid induced normal grow th (type 3 sweetpotato). but the acidic charge isomers were suppressed . Combined supplementation with benzyladenine and naphthaleneacetic ac id suppressed all the charge isomers and abolished amination by the en zyme, thereby causing severe growth retardation. The type 1 and type 3 sweetpotato glutamate dehydrogenases were more aminating (Michaelis c onstant K-m = 12.5 and 14.8 mM NH4Cl, respectively) than type 2 sweetp otato glutamate dehydrogenase (K-m = 82.6 mM NH4Cl). The differential growth retardations which accompanied the three phases of the suppress ion of the aminating charge isomers are evidence that the enzyme is am inating in vivo and that it employed that activity in the regulation o f sweetpotato growth and differentiation.