Three classes of 5-fluorpyrimidine-resistant mutants of Diplococcus pneumoniae have been characterized. The mutant strain upp is resistant to high concentrations of the fluoropyrimidine bases fluorouracil (FU) and fluorocytosine (FC); strain upp has a defective uridine monophosphate pyrophosphorylase. The mutant strain udk is resistant to inhibition by fluorouridine (FUR) and exhibits defective uridine kinase activity. The mutant strain fun is resistant to inhibition by the nucleosides fluorodeoxyuridine, fluorodeoxycytidine, and FUR, but shows normal activity for all pyrimidine pathway enzymes tested. This strain may be defective in the activity of a transport system that governs the cellular uptake of pyrimidine ribo- and deoxyribonucleosides. Biochemical studies on wild-type and fluoropyrimidine-resistant pneumococci are discussed with respect to the transport and early metabolism of preformed pyrimidine precursors by this organism.
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机译：表征了三类肺炎双球菌的5-氟嘧啶抗性突变体。突变株 upp 对高浓度的氟嘧啶碱基氟尿嘧啶（FU）和氟胞嘧啶（FC）具有抗性。 upp 菌株的尿苷单磷酸焦磷酸化酶有缺陷。突变株 udk 对氟尿苷（FUR）的抑制具有抗性，并显示出缺陷的尿苷激酶活性。突变株 fun 对核苷氟代脱氧尿苷，氟代脱氧胞苷和FUR具有抑制作用，但对所有测试的嘧啶途径酶均显示正常活性。该菌株在控制嘧啶核糖核苷和脱氧核糖核苷的细胞摄取的运输系统的活性中可能是缺陷的。关于野生型和耐氟嘧啶的肺炎球菌的生化研究，涉及该生物对预制嘧啶前体的转运和早期代谢。
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