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恶臭假单胞菌α-酮己二酸途径中酶诱导的遗传控制:cat突变的缺失定位

Genetic control of enzyme induction in the -ketoadipate pathway of Pseudomonas putida: deletion mapping of cat mutations.

作者信息

Wheelis M L, Ornston L N

出版信息

J Bacteriol. 1972 Feb;109(2):790-5. doi: 10.1128/jb.109.2.790-795.1972.

Abstract

A number of spontaneous mutant strains of Pseudomonas putida, obtained by repeated selection for inability to grow with cis,cis-muconate, have been shown to carry deletions in catB, the structural gene for muconate lactonizing enzyme. These strains have been employed for deletion mapping of the genetic region containing catB and catC (the structural gene for muconolactone isomerase, the synthesis of which is coordinate with that of muconate lactonizing enzyme). All deletions that overlap mutant sites located on the left side of the genetic map, as well as the point mutations in that region, lead to a pleiotropic loss of both catB and catC activities. We propose that this region to the left of catB has a regulatory function. Although the details of regulation at the molecular level are unclear, our data indicate that catB and catC may well be controlled by a mechanism unlike any yet described by workers on enteric bacteria.

摘要

通过反复筛选不能利用顺,顺-粘康酸生长而获得的多个恶臭假单胞菌自发突变株,已被证明在粘康酸内酯化酶的结构基因catB中存在缺失。这些菌株已被用于对包含catB和catC(粘康酸内酯异构酶的结构基因,其合成与粘康酸内酯化酶的合成是协同的)的遗传区域进行缺失定位。所有与位于遗传图谱左侧的突变位点重叠的缺失以及该区域的点突变,都会导致catB和catC活性的多效性丧失。我们提出catB左侧的这个区域具有调节功能。尽管在分子水平上调节的细节尚不清楚,但我们的数据表明,catB和catC很可能受一种与肠道细菌研究人员迄今所描述的任何机制都不同的机制控制。

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