REGULATION OF BETA-GLUCOSIDE SYSTEM IN ESCHERICHIA-COLI K-12
REGULATION OF BETA-GLUCOSIDE SYSTEM IN ESCHERICHIA-COLI K-12
复制标题
DOI：
10.1128/jb.120.2.638-650.1974
复制
发表时间：
1974-01-01
影响因子：
3.2
通讯作者：
SCHAEFLER, S
中科院分区：
文献类型：
--
作者：
PRASAD, I;SCHAEFLER, S
在大肠杆菌野生型细胞中，β-葡萄糖苷调节基因 (bglR+tobglR−) 的突变导致诱导型磷酸-β-葡萄糖苷酶 B (bglB+) 和 β-葡萄糖苷特异性酶 II 种类（β-葡萄糖苷转运 I [bglC+]）同时表达；额外的突变（bglS+tobglS4）允许这些酶组成型形成。 bglalleles已按以下顺序进行映射：pyrE、bglA、bglB、bglS、bglR、bglC、ilvD。调节等位基因（bglR−tobglR+）的回复突变导致bglB+、bglS+或bglS4、bglC+等位基因表达停止。然而，具有bglB+、bglS4、bglR8、bglC+等位基因的菌株中位于bglS4和bglR8等位基因之间的位点的突变允许bglS4和bglB+等位基因的表达，但对bglC+等位基因的表达没有影响。这表明突变具有启动子型功能，在缺乏调节等位基因功能(bglR8)的情况下，仅更新bglS4和bglB+等位基因的功能。互补研究表明，bglB+、bglS+或bglS4、bglC+等位基因仅在bglR-等位基因的切缝处表达。在组成型菌株（bglB+、bglS4、bglR-、bglC+）中，表达的bglS4等位基因形成可溶性产物，该产物在bglB+和bglC+等位基因反式中起作用，并且仅当bglB+和bglC+等位基因与bglR-等位基因切开表达时才显得有效。由此表明，磷酸-β-葡萄糖苷酶B和β-葡萄糖苷转运I的组成型生物合成处于正控制之下。由于调节等位基因 bglR− 位于 bglS4 和 bglC+ 等位基因之间，并且以顺式作用，因此突变 (bglR+tobglR−) 似乎允许在一个方向上启动转录以表达 bglS4、bglB+ 等位基因，并在另一个方向上启动转录以表达 bglC+ 等位基因。结构基因bglB和bglC与调节基因bglR和bglS相邻，结构基因受调节基因协调控制。因此，建议bglB、bglS、bglR、bglC基因形成abgloperon。
InEscherichia coliwild-type cells, a mutation at the β-glucoside regulatory gene (bglR+tobglR−) leads to simultaneous expression of inducible phospho-β-glucosidase B (bglB+) and a β-glucoside-specific species of enzyme II (β-glucoside transport I [bglC+]); an additional mutation (bglS+tobglS4) allows these enzymes to be formed constitutively. Thebglalleles have been mapped in the following order:pyrE, bglA, bglB, bglS, bglR, bglC, ilvD. The back mutation in the regulatory allele (bglR−tobglR+) caused the cessation of the expression of thebglB+,bglS+orbglS4, bglC+alleles. However, a mutation in a strain withbglB+,bglS4, bglR8, bglC+alleles, at theinisite that lies between thebglS4and thebglR8allele, allowed the expression of thebglS4andbglB+alleles, but showed no affect on the expression of thebglC+allele. It is suggested that theinimutation possesses a promotor-type function that in the absence of regulatory allele function (bglR8) renews the functioning of only thebglS4andbglB+alleles. The complementation studies have shown that thebglB+,bglS+orbglS4, bglC+alleles are expressed only incisto thebglR−allele. In the constitutive strain (bglB+,bglS4, bglR−,bglC+), the expressedbglS4allele formed a soluble product that acts intransover thebglB+andbglC+alleles and that appears effective only when thebglB+and thebglC+alleles are expressed incisto thebglR−allele. It thus showed that the constitutive biosynthesis of phospho-β-glucosidase B and β-glucoside transport I is under positive control. Since the regulatory allelebglR−lies between thebglS4and theblgC+alleles, and acts incis, it appears that the mutation (bglR+tobglR−) allows the initiation of transcription in one direction to express thebglS4, bglB+alleles and in the other to express thebglC+allele. The structural genesbglBandbglClie adjacent to the regulatory genesbglRandbglS, and the structural genes are coordinately controlled by the regulatory genes. It is, therefore, proposed that thebglB, bglS, bglR, bglCgenes form abgloperon.