Narang Atul, Oehler Stefan
Department of Biochemical Engineering and Biotechnology, Indian Institute of Technology Delhi, Hauz Khas, New Delhi, India.
Department of Biochemical Engineering and Biotechnology, Indian Institute of Technology Delhi, Hauz Khas, New Delhi, India
J Bacteriol. 2017 Apr 11;199(9). doi: 10.1128/JB.00796-16. Print 2017 May 1.
The (lactose) operon (which processes β-galactosides) and the (melibiose) operon (which processes α-galactosides) of have a close historical connection. A number of shared substrates and effectors of the permeases and regulatory proteins have been reported over the years. Until now, β-thiogalactosides like TMG (methyl-β-d-thiogalactopyranoside) and IPTG (isopropyl-β-d-thiogalactopyranoside) have not generally been considered to be inducers of the operon. The same is true for β-galactosides such as lactose [β-d-galactopyranosyl-(1→4)-d-glucose], which is a substrate but is not itself an inducer of the operon. This report shows that all three sugars can induce the operon significantly when they are accumulated in the cell by Lac permease. Strong induction by β-thiogalactosides is observed in the presence of Lac permease, and strong induction by lactose (more than 200-fold) is observed in the absence of β-galactosidase. This finding calls for reevaluation of TMG uptake experiments as assays for Lac permease that were performed with strains. The typical textbook picture of bacterial operons is that of stand-alone units of genetic information that perform, in a regulated manner, well-defined cellular functions. Less attention is given to the extensive interactions that can be found between operons. Well-described examples of such interactions are the effector molecules shared by the and operons. Here, we show that this set has to be extended to include β-galactosides, which have been, until now, considered not to effect the expression of the operon. That they can be inducers of the operon as well as the operon has not been noted in decades of research because of the genetic background used in previous studies.
大肠杆菌的乳糖操纵子(处理β-半乳糖苷)和蜜二糖操纵子(处理α-半乳糖苷)有着密切的历史联系。多年来,已经报道了一些通透酶和调节蛋白的共享底物及效应物。到目前为止,像TMG(甲基-β-D-硫代半乳糖吡喃糖苷)和IPTG(异丙基-β-D-硫代半乳糖吡喃糖苷)这样的β-硫代半乳糖苷一般不被认为是乳糖操纵子的诱导物。对于像乳糖[β-D-吡喃半乳糖基-(1→4)-D-葡萄糖]这样的β-半乳糖苷也是如此,它是一种底物,但本身不是乳糖操纵子的诱导物。本报告表明,当这三种糖通过乳糖通透酶在细胞中积累时,它们都能显著诱导乳糖操纵子。在存在乳糖通透酶的情况下观察到β-硫代半乳糖苷的强烈诱导作用,在不存在β-半乳糖苷酶的情况下观察到乳糖的强烈诱导作用(超过200倍)。这一发现要求重新评估用大肠杆菌菌株进行的作为乳糖通透酶测定的TMG摄取实验。细菌操纵子的典型教科书描述是作为独立的遗传信息单元,以一种受调控的方式执行明确的细胞功能。人们较少关注操纵子之间广泛的相互作用。这种相互作用的详细例子是乳糖操纵子和蜜二糖操纵子共享的效应分子。在这里,我们表明这个集合必须扩展到包括β-半乳糖苷,直到现在,β-半乳糖苷一直被认为不会影响乳糖操纵子的表达。由于以前研究中使用的大肠杆菌遗传背景,在几十年的研究中都没有注意到它们可以是乳糖操纵子以及蜜二糖操纵子的诱导物。