Indole-mediated cell division control by plasmid ColE1
质粒 ColE1 吲哚介导的细胞分裂控制
基本信息
- 批准号:BB/F002912/1
- 负责人:
- 金额:$ 40.71万
- 依托单位:
- 依托单位国家:英国
- 项目类别:Research Grant
- 财政年份:2007
- 资助国家:英国
- 起止时间:2007 至 无数据
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
The bacterium Escherichia coli is responsible for severe human food poisoning (e.g. strain O157) and is also used widely in the laboratory as a 'model organism'. It is relatively simple, having about 4000 genes which reside on a single circular DNA molecule or chromosome. Extra genes, which may give the bacterium the ability to cause disease or to be resistant to antibiotics, are often found on smaller DNA molecules known as plasmids. As the bacterium grows and divides these plasmids are copied and are distributed to new bacterial cells. Occasionally the plasmids are damaged and fuse together in pairs known as dimers. These dimers interfere with the distribution of plasmids to daughter cells when the bacterium divides and so cause loss of the plasmid from its bacterial host. To avoid plasmid loss it is important that the damage is repaired. The main repair process involves cutting the dimers into two (by a process known as site-specific recombination), thus restoring them to their original form. This is not, however, the whole story. The plasmid also activates a mechanism which prevents the bacterial cell from dividing while plasmid repair is taking place. This type of response to DNA damage called a 'checkpoint' and although it is well-known in more complex organisms, such as fruit flies or humans, is less common in bacteria. We are interested in exactly how the plasmid stops its bacterial host dividing. We have known for some time that the mechanism involves the production of a small RNA molecule called Rcd but we have not known exactly what Rcd does. Recently we discovered that Rcd binds to an enzyme in the bacterial cell and stimulates it to produce a small organic molecule called indole. We have shown that it is indole which is responsible for stopping the division of the bacterial cell. In this project we propose to look in detail at exactly how Rcd causes the enzyme to make indole and try to understand, at a molecular level, how indole stops E. coli dividing. Understanding this process is important not only because it illustrates an important way in which bacterial and plasmids deal with DNA damage, but also because developing drugs which interfere with this process could potentially provide a new antibiotics to fight bacterial infection.
大肠杆菌是导致严重人类食物中毒的细菌(例如菌株O157),也被广泛用作实验室中的“模式生物”。它相对简单,有大约4000个基因,位于单个环状DNA分子或染色体上。额外的基因,可能使细菌能够引起疾病或对抗生素产生抗药性,通常存在于称为质粒的较小DNA分子上。随着细菌的生长和分裂,这些质粒被复制并分布到新的细菌细胞中。有时质粒被破坏并成对融合在一起,称为二聚体。当细菌分裂时,这些二聚体干扰质粒向子细胞的分布,从而导致质粒从其细菌宿主中丢失。为了避免质粒丢失,重要的是修复损伤。主要的修复过程包括将二聚体切割成两个(通过一种称为位点特异性重组的过程),从而将它们恢复到原始形式。然而,这并不是故事的全部。质粒还激活一种机制,在质粒修复发生时阻止细菌细胞分裂。这种对DNA损伤的反应称为“检查点”,尽管它在更复杂的生物体中是众所周知的,如果蝇或人类,但在细菌中不太常见。我们感兴趣的是质粒究竟是如何阻止其细菌宿主分裂的。我们已经知道了一段时间,该机制涉及一种称为Rcd的小RNA分子的产生,但我们还不知道Rcd的确切作用。最近,我们发现Rcd与细菌细胞中的一种酶结合,并刺激它产生一种称为吲哚的有机小分子。我们已经证明,是吲哚负责停止细菌细胞的分裂。在这个项目中,我们建议详细研究Rcd是如何引起酶产生吲哚的,并试图在分子水平上了解吲哚是如何阻止E。大肠杆菌分裂。了解这一过程很重要,不仅因为它说明了细菌和质粒处理DNA损伤的重要方式,而且还因为开发干扰这一过程的药物可能会提供一种新的抗生素来对抗细菌感染。
项目成果
期刊论文数量(10)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Local and Universal Action: The Paradoxes of Indole Signalling in Bacteria.
- DOI:10.1016/j.tim.2020.02.007
- 发表时间:2020-07
- 期刊:
- 影响因子:15.9
- 作者:Ashraf Zarkan;Junyan Liu;M. Matuszewska;Hannah Gaimster;D. Summers
- 通讯作者:Ashraf Zarkan;Junyan Liu;M. Matuszewska;Hannah Gaimster;D. Summers
The indole pulse: a new perspective on indole signalling in Escherichia coli.
- DOI:10.1371/journal.pone.0093168
- 发表时间:2014
- 期刊:
- 影响因子:3.7
- 作者:Gaimster H;Cama J;Hernández-Ainsa S;Keyser UF;Summers DK
- 通讯作者:Summers DK
The effect of bacterial signal indole on the electrical properties of lipid membranes.
- DOI:10.1002/cphc.201200793
- 发表时间:2013-02-04
- 期刊:
- 影响因子:0
- 作者:Chimerel C;Murray AJ;Oldewurtel ER;Summers DK;Keyser UF
- 通讯作者:Keyser UF
Regulation of Indole Signalling during the Transition of E. coli from Exponential to Stationary Phase.
- DOI:10.1371/journal.pone.0136691
- 发表时间:2015
- 期刊:
- 影响因子:3.7
- 作者:Gaimster H;Summers D
- 通讯作者:Summers D
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David Keith Summers的其他文献
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{{ truncateString('David Keith Summers', 18)}}的其他基金
Quiescent Microbial Cell Factories
静止微生物细胞工厂
- 批准号:
BB/N010256/1 - 财政年份:2016
- 资助金额:
$ 40.71万 - 项目类别:
Research Grant
Rescuing Antibiotics from Bacterial Resistance
拯救抗生素免受细菌耐药性
- 批准号:
BB/M015394/1 - 财政年份:2015
- 资助金额:
$ 40.71万 - 项目类别:
Research Grant
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