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deo操纵子的特性:在胸腺嘧啶利用中的作用及对脱氧核苷的敏感性

Characteristics of the deo operon: role in thymine utilization and sensitivity to deoxyribonucleosides.

作者信息

Lomax M S, Greenberg G R

出版信息

J Bacteriol. 1968 Aug;96(2):501-14. doi: 10.1128/jb.96.2.501-514.1968.

Abstract

Inability to grow on deoxyribonucleosides as the sole carbon source is characteristic of deo mutants of Escherichia coli. Growth of deoC mutants, which lack deoxyribose 5-phosphate aldolase, is reversibly inhibited by deoxyribonucleosides through inhibition of respiration. By contrast, deoB mutants are not sensitive to deoxyribonucleosides, and deoxyribose 5-phosphate aldolase and thymidine phosphorylase are present at normal levels but are not inducible by thymidine. Organisms with the genotype deoB(-)thy(-) or deoC(-)thy(-) are able to grow on low levels of thymine, whereas deoB(+)thy(-) or deoC(+)thy(-) strains require high levels of thymine for growth. The deoB and deoC mutations are transducible with and map on the counterclockwise side of the threonine marker. They are closely linked to deoA, a gene determining thymidine phosphorylase. Merodiploids heterozygous for either the deoB or deoC genes are resistant to deoxyribonucleosides and, in combination with the thy mutation, require high levels of thymine for growth. Cultures of thy(+)deoC(-) mutants are inhibited by thymidine until this compound has been completely degraded and excreted as deoxyribose and thymine, whereupon growth promptly resumes at a normal rate. The inhibition of respiration in deoC strains and the induction of thymidine phosphorylase and deoxyribose 5-phosphate aldolase in the wild-type organism are considered to result from the accumulation of deoxyribose 5-phosphate.

摘要

无法以脱氧核糖核苷作为唯一碳源生长是大肠杆菌deo突变体的特征。缺乏脱氧核糖5-磷酸醛缩酶的deoC突变体的生长会被脱氧核糖核苷通过抑制呼吸作用而可逆地抑制。相比之下,deoB突变体对脱氧核糖核苷不敏感,脱氧核糖5-磷酸醛缩酶和胸苷磷酸化酶的水平正常,但不能被胸苷诱导。基因型为deoB(-)thy(-)或deoC(-)thy(-)的生物体能够在低水平的胸腺嘧啶上生长,而deoB(+)thy(-)或deoC(+)thy(-)菌株生长需要高水平的胸腺嘧啶。deoB和deoC突变可被转导,并且定位于苏氨酸标记的逆时针一侧。它们与决定胸苷磷酸化酶的基因deoA紧密连锁。对deoB或deoC基因杂合的部分二倍体对脱氧核糖核苷具有抗性,并且与thy突变结合时,生长需要高水平的胸腺嘧啶。thy(+)deoC(-)突变体的培养物会被胸苷抑制,直到该化合物完全降解并以脱氧核糖和胸腺嘧啶的形式排出,随后生长迅速以正常速率恢复。deoC菌株中呼吸作用的抑制以及野生型生物体中胸苷磷酸化酶和脱氧核糖5-磷酸醛缩酶的诱导被认为是由脱氧核糖5-磷酸的积累导致的。

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