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大肠杆菌对L-阿拉伯糖敏感、缺乏5-磷酸-L-核酮糖4-差向异构酶的突变体

L-Arabinose-sensitive, L-ribulose 5-phosphate 4-epimerase-deficient mutants of Escherichia coli.

作者信息

ENGLESBERG E, ANDERSON R L, WEINBERG R, LEE N, HOFFEE P, HUTTENHAUER G, BOYER H

出版信息

J Bacteriol. 1962 Jul;84(1):137-46. doi: 10.1128/jb.84.1.137-146.1962.

Abstract

Englesberg, E. (University of Pittsburgh, Pittsburgh, Pa.), R L. Anderson, R. Weinberg, N. Lee, P. Hoffee, G. Huttenhauer, and H. Boyer. l-Arabinose-sensitive, l-ribulose 5-phosphate 4-epimerase-deficient mutants of Escherichia coli. J. Bacteriol. 84:137-146. 1962-l-Arabinose-negative mutants of Escherichia coli B/r, ara-53 and ara-139, are deficient in the enzyme l-ribulose 5-phosphate 4-epimerase; ara-53, further analyzed, accumulates large quantities of l-ribulose 5-phosphate when incubated with l-arabinose. The mutant sites are closely linked to the left of the previously ordered l-arabinose mutant sites, and probably represent the structural gene for l-ribulose 5-phosphate 4-epimerase (gene D) in the l-arabinose operon. The inducible levels of l-arabinose isomerase and l-ribulose 5-phosphate 4-epimerase vary correspondingly as a result of mutation in the structural gene for l-ribulokinase (gene B), further substantiating the dual structural and regulatory function of this gene locus. Ara-53 and ara-139 are strongly inhibited by l-arabinose and give rise to l-arabinose-resistant mutants. The one resistant mutant analyzed still lacks the 4-epimerase but is deficient in l-ribulokinase and has increased l-arabinose isomerase activity, a characteristic of a type of mutation in the B gene. It is proposed that accumulation of l-ribulose 5-phosphate is responsible for the inhibition, and that mutation to resistance will involve mutation in the A, B, C, permease, or repressor genes, thus providing a direct method for isolating these types of l-arabinose-negative mutants. Glucose prevents and cures the l-arabinose inhibition.

摘要

恩格尔斯伯格,E.(匹兹堡大学,宾夕法尼亚州匹兹堡),R.L.安德森,R.温伯格,N.李,P.霍费,G.胡滕豪尔,和H.博耶。大肠杆菌的L-阿拉伯糖敏感、5-磷酸-L-核酮糖4-差向异构酶缺陷型突变体。《细菌学杂志》84:137 - 146。1962年 - 大肠杆菌B/r的L-阿拉伯糖阴性突变体ara-53和ara-139缺乏5-磷酸-L-核酮糖4-差向异构酶;进一步分析的ara-53在与L-阿拉伯糖一起孵育时会积累大量的5-磷酸-L-核酮糖。突变位点与先前排列的L-阿拉伯糖突变位点紧密连锁在左侧,可能代表L-阿拉伯糖操纵子中5-磷酸-L-核酮糖4-差向异构酶(基因D)的结构基因。由于5-磷酸-L-核酮糖激酶(基因B)的结构基因突变,L-阿拉伯糖异构酶和5-磷酸-L-核酮糖4-差向异构酶的诱导水平相应变化,进一步证实了该基因座的双重结构和调节功能。Ara-53和ara-139受到L-阿拉伯糖的强烈抑制,并产生L-阿拉伯糖抗性突变体。分析的一个抗性突变体仍然缺乏4-差向异构酶,但缺乏5-磷酸-L-核酮糖激酶且L-阿拉伯糖异构酶活性增加,这是B基因中一种突变类型的特征。有人提出5-磷酸-L-核酮糖的积累是抑制的原因,而抗性突变将涉及A、B、C、通透酶或阻遏基因的突变,从而提供了一种分离这些类型的L-阿拉伯糖阴性突变体的直接方法。葡萄糖可预防和解除L-阿拉伯糖的抑制作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1369/277779/50319de8bb81/jbacter00459-0160-a.jpg

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