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Regulation by Auxin of Carbohydrate Metabolism Involved in Cell Wall Synthesis by Pea Stem Tissue ¹

^a Market Quality Research Division, United States Department of Agriculture, Beltsville, Maryland 20705, Department of Biological Sciences, Stanford University, Stanford, California 94305

Promotion of cell wall synthesis (from glucose) in pea (Pisum sativum) stem segments by indoleacetic acid (IAA) develops over a period of 1 to 2 hours and is comprised of a promotion of glucose uptake plus a promotion of the utilization of absorbed glucose. The effect of IAA resembles, in these and other respects, its effect on cell wall synthesis in oat coleoptile segments, but the pea system differs in not being inhibited by galactose or mannose, in involving considerably more isotope dilution by endogenous substrates, and in certain other respects.

Effector influences upon and total activities of the following enzymes obtained from etiolated pea stem segments pretreated with or without IAA were examined: phosphoglucomutase, uridine diphosphate glucose (UDP-glucose) pyrophosphorylase, nucleoside diphosphokinase, UDP-glucose dehydrogenase, inorganic pyrophosphatase, hexokinase (particulate and soluble), and UDP-glucose--1,4-glucan-glucosyl transferase (-glucan synthetase). The first three enzymes mentioned exhibit high activity relative to the flux in vivo, do not appear to show physiologically significant effector responses, and are concluded not to be control points. UDP-glucose dehydrogenase activity is regulated by UDP-xylose. Hexokinase is a potential control point but does not exhibit regulatory effects related to the IAA response. -Glucan synthetase is the only one of these enzymes with activity which is increased by treatment of tissue with IAA, and this may be responsible for the effect of IAA on wall synthesis.

Assays of metabolite pools support the conclusion that stimulation of polysaccharide synthesis by IAA is due partly to changes in hexokinase reaction rate resulting from an increase in metabolic glucose pool size caused by increased glucose uptake, and partly to increased activity at the polysaccharide synthetase level.