A labile serum-dependent uridine uptake function in mouse embryo cells

Abstract

Stimulation of uridine uptake in serum-less mouse embryo cells by serum repletion has been shown to require the continual presence of serum for maintenance of maximum activity. Removal of serum terminates further stimulation and is followed by a rapid decay of uptake capacity characterized by a 2–4-fold decrease in V with no change in the apparent K m of the reaction. Acquisition of uptake capacity is sensitive to inhibitors of both RNA (actinomycin D) and protein (cycloheximide) synthesis. Insulin is shown to substitute for serum in the stimulation of uridine uptake in serum-less cells. Levels of uridine kinase activity do not correlate with uptake capacity in response to either serum or metabolic inhibitors, suggesting that this enzyme is not responsible for the control of uptake. It is proposed that uridine uptake in mouse embryo cells is controlled by a labile system which requires input from the extra-cellular environment to maintain functional capacity. The identity of the rate-limiting process is not known at this time, but is postulated to be some part of the carrier system.