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本文引用的文献

1
Glucose transporter mutants of Escherichia coli K-12 with changes in substrate recognition of IICB(Glc) and induction behavior of the ptsG gene.大肠杆菌K-12的葡萄糖转运体突变体，其IICB(Glc)的底物识别和ptsG基因的诱导行为发生了变化。
J Bacteriol. 2000 Aug;182(16):4443-52. doi: 10.1128/JB.182.16.4443-4452.2000.
2
Substrate specificity and signal transduction pathways in the glucose-specific enzyme II (EII(Glc)) component of the Escherichia coli phosphotransferase system.大肠杆菌磷酸转移酶系统中葡萄糖特异性酶II（EII(Glc)）组分的底物特异性和信号转导途径。
J Bacteriol. 2000 Aug;182(16):4437-42. doi: 10.1128/JB.182.16.4437-4442.2000.
3
SsrA-mediated tagging and proteolysis of LacI and its role in the regulation of lac operon.SsrA介导的LacI标签化与蛋白水解作用及其在乳糖操纵子调控中的作用。
EMBO J. 2000 Jul 17;19(14):3762-9. doi: 10.1093/emboj/19.14.3762.
4
Dynamic spatial regulation in the bacterial cell.细菌细胞中的动态空间调控
Cell. 2000 Jan 7;100(1):89-98. doi: 10.1016/s0092-8674(00)81686-4.
5
Negative regulation of the pts operon by Mlc: mechanism underlying glucose induction in Escherichia coli.Mlc对磷酸转移酶系统操纵子的负调控：大肠杆菌中葡萄糖诱导的潜在机制。
Genes Cells. 1999 Jul;4(7):391-9. doi: 10.1046/j.1365-2443.1999.00268.x.
6
Purification of Mlc and analysis of its effects on the pts expression in Escherichia coli.Mlc的纯化及其对大肠杆菌中pts表达影响的分析。
J Biol Chem. 1999 Sep 3;274(36):25398-402. doi: 10.1074/jbc.274.36.25398.
7
Expression of the phosphotransferase system both mediates and is mediated by Mlc regulation in Escherichia coli.磷酸转移酶系统的表达在大肠杆菌中介导并受Mlc调控。
Mol Microbiol. 1999 Jul;33(2):260-73. doi: 10.1046/j.1365-2958.1999.01462.x.
8
Elucidation of a PTS-carbohydrate chemotactic signal pathway in Escherichia coli using a time-resolved behavioral assay.利用时间分辨行为分析阐明大肠杆菌中的磷酸转移酶系统-碳水化合物趋化信号通路。
Mol Biol Cell. 1999 Apr;10(4):1133-46. doi: 10.1091/mbc.10.4.1133.
9
The ATP-binding cassette subunit of the maltose transporter MalK antagonizes MalT, the activator of the Escherichia coli mal regulon.麦芽糖转运蛋白MalK的ATP结合盒亚基可拮抗MalT，后者是大肠杆菌麦芽糖操纵子的激活因子。
Mol Microbiol. 1998 Nov;30(3):535-46. doi: 10.1046/j.1365-2958.1998.01084.x.
10
A global repressor (Mlc) is involved in glucose induction of the ptsG gene encoding major glucose transporter in Escherichia coli.一种全局阻遏物（Mlc）参与了大肠杆菌中编码主要葡萄糖转运蛋白的ptsG基因的葡萄糖诱导过程。
Mol Microbiol. 1998 Sep;29(6):1509-19. doi: 10.1046/j.1365-2958.1998.01035.x.

大肠杆菌葡萄糖转运蛋白的一种新调控作用：全局阻遏物Mlc的膜隔离

A novel regulatory role of glucose transporter of Escherichia coli: membrane sequestration of a global repressor Mlc.

作者信息

Tanaka Y, Kimata K, Aiba H

机构信息

Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa, Nagoya 464-8602, Japan.

出版信息

EMBO J. 2000 Oct 16;19(20):5344-52. doi: 10.1093/emboj/19.20.5344.

DOI:10.1093/emboj/19.20.5344
PMID:11032802
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC314007/
Abstract

External glucose stimulates transcription of several genes including ptsG encoding IICB(Glc), a membrane component of the phosphotransferase system (PTS), by relieving the negative regulation of a global repressor Mlc in Escherichia coli. We investigate here how glucose modulates Mlc action. The Mlc-mediated repression is eliminated by a ptsI mutation, while Mlc is constitutively active in a ptsG mutant. We show that IICB(Glc)-FLAG interacts physically with Mlc in crude extracts prepared from cells in which IICB(Glc) is supposed to exist as the non-phosphorylated form. The IICB(Glc)-Mlc interaction is no longer observed when IICB(Glc) is phosphorylated. Exogenously added purified Mlc binds to purified IICB(Glc)-FLAG. We also demonstrate that Mlc is associated with membrane when IICB(Glc) is dephosphorylated while it is in the cytoplasm when IICB(Glc) is phosphorylated or absent. We conclude that IICB(Glc) regulates the cellular localization of Mlc, depending on its phosphorylation state, which is determined by the availability of external glucose. Thus, glucose induces the transcription of Mlc-regulated promoters by sequestering Mlc to the membrane through dephosphorylation of IICB(Glc).

摘要

胞外葡萄糖通过解除大肠杆菌中全局阻遏物Mlc的负调控作用，刺激包括编码磷酸转移酶系统（PTS）膜成分IICB(Glc)的ptsG在内的多个基因的转录。我们在此研究葡萄糖如何调节Mlc的作用。ptsI突变可消除Mlc介导的阻遏作用，而在ptsG突变体中Mlc呈组成型激活。我们发现，在假定IICB(Glc)以非磷酸化形式存在的细胞制备的粗提物中，IICB(Glc)-FLAG与Mlc存在物理相互作用。当IICB(Glc)磷酸化时，不再观察到IICB(Glc)-Mlc相互作用。外源添加的纯化Mlc可与纯化的IICB(Glc)-FLAG结合。我们还证明，当IICB(Glc)去磷酸化时，Mlc与膜相关，而当IICB(Glc)磷酸化或不存在时，Mlc位于细胞质中。我们得出结论，IICB(Glc)根据其磷酸化状态调节Mlc的细胞定位，而磷酸化状态由胞外葡萄糖的可用性决定。因此，葡萄糖通过IICB(Glc)的去磷酸化将Mlc隔离到膜上，从而诱导Mlc调控启动子的转录。