Previous work has provided evidence that plants may require boron to maintain adequate levels of pynmidine nucleotides, suggesting that the state of boron deficiency may actually be one of pyrimidine starvation. Since the avaflability of pyrimidine nucleotides is influenced by their rates of synthesis, salvage, and catabolism, we compared these activities in the terminal 3 centimeters of roots excised from boron-deficient and -sufficient squash plants (Cscurbita pepo L. (7) and [14CJorotic acid (36) into RNA in borondeficient mung bean root apices and cotton ovules, respectively. These reports suggest that the utilization or the level of available purine or pyrimidine nucleotides, or both, is altered by boron deprivation.We were particularly interested in the observation (30) that plants growing in the absence of boron could be protected from developing boron-deficiency symptoms by adding a hydrolysate of yeast RNA to the nutrient solution. Work in our laboratory (2, 15, 16), and elsewhere (4, 5) tested the effects of both purine and pyrimidine bases on plant growth to determine which component(s) of the RNA hydrolysate afforded this protection. Intact plants and isolated organs cultured in the absence of boron were protected to varying degrees from developing boron deficiency symptoms when pyrimidine bases were added to the medium.This result was taken as evidence that the state of boron deficiency may, in fact, be a case of pyrimidine starvation. Such an interpretation was supported by the observations that both barbituric acid and 6-azauracil, known inhibitors of pyrimidine biosynthesis (13,25,26), produced symptoms identical with those of boron deprivation (2, 5, 16). Various investigators (5,(19)(20)(21)36) have suggested that boron deficiency results in impaired de novo biosynthesis of pyrimidine nucleotides. Such impairment could occur through either a loss in amount of one or more enzymes or enhanced sensitivity of the de novo pathway to end product inhibition. Starvation for pyrimidine nucleotides could also result from an inability of boron-deficient plants to salvage or reutilize pyrimidine bases or nucleosides, or from an acceleration of pyrimidine catabolism.In this communication, we report the results of a comparison of the capacity of roots from boron-sufficient (+B)3 and borondeficient (-B) squash plants (Cucurbita pepo L., cv. Early Prolific straightneck) to synthesize uridine nucleotides de novo. We also include an examination of the possibility that boron deprivation interferes with the mechanism regulating the de novo pathway through end product inhibition. In addition, since catabolism opposes de novo biosynthesis, we also assessed the capacity of +B and -B roots to catabolize uridine and uracil. Finally, we measured salvage activity for the reutilization of pyrimidines during these two states of boron nutrition.