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[大肠杆菌K-12胸苷磷酸化酶缺失突变体表型回复性质的进一步研究]

[A further study of the nature of phenotypical reversions in thymidine phosphorylase deletion mutants of Escherichia coli K-12].

作者信息

Mironov A S, Smirnov Iu V, Sukhodolets V V

出版信息

Genetika. 1975 Apr;11(4):97-105.

PMID:776741
Abstract

Thymidine dependent (thy) strains of Escherichia coli carrying deletions for thymidine phosphorylase (tpp gene) formed phenotypical reversions for the ability of growth at the medium containing thymine as a source of thymidilate. The ability of the thy tpp strains to utilyze thymine for growth is due to mutations of the regulatory genes cytR and udpR, which control the uridine phosphorylase activity. This enzyme in constitutive amounts catalyzes conversion of thymine to thymidine in bacterial cells with a block of deoxyribose catabolism (deoxyribomutase-negative strains). The udpR mutant by contrast to cytR mutants reported by Munch-Petersen et al. (1972) are shown to contain low, inducible levels of cytidine deaminase and deo-enzymes. The udpR mutation is recessive with respect to wild type allele. It is supposed that the product of udpR gene is a specific repressor of uridine phosphorylase (udp) gene. The udpR mutation is closely linked (90% contransduction) to uridine phosphorylase (udp) gene, and is located approximately at 75 min, on the E. coli chromosome.

摘要

携带胸苷磷酸化酶缺失(tpp基因)的大肠杆菌胸腺嘧啶依赖型(thy)菌株,在以胸腺嘧啶作为胸苷酸来源的培养基上形成了生长能力的表型回复。thy tpp菌株利用胸腺嘧啶生长的能力归因于调控基因cytR和udpR的突变,这两个基因控制尿苷磷酸化酶的活性。在具有脱氧核糖分解代谢阻断的细菌细胞(脱氧核糖突变酶阴性菌株)中,该酶以组成型量催化胸腺嘧啶转化为胸苷。与Munch-Petersen等人(1972年)报道的cytR突变体相反,udpR突变体显示含有低水平的、可诱导的胞苷脱氨酶和脱氧酶。udpR突变相对于野生型等位基因是隐性的。推测udpR基因的产物是尿苷磷酸化酶(udp)基因的特异性阻遏物。udpR突变与尿苷磷酸化酶(udp)基因紧密连锁(共转导率90%),并且位于大肠杆菌染色体上大约75分钟处。

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