Chemotaxis towards autoinducer 2 mediates autoaggregation in Escherichia coli.
Chemotaxis towards autoinducer 2 mediates autoaggregation in Escherichia coli.
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DOI：
10.1038/ncomms12984
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发表时间：
2016-09-30
影响因子：
16.6
通讯作者：
Sourjik, Victor
中科院分区：
文献类型：
--
作者：
Laganenka, Leanid;Colin, Remy;Sourjik, Victor
细菌通过产生和感知称为自体诱导物的细胞外信号分子进行交流。这种被称为群体感应的细胞间信号传递允许细菌在高细胞密度下协调和同步行为反应。自体诱导物2(AI-2)是目前已知的唯一一种由大肠杆菌产生的群体感应分子，但其生理功能尚不清楚，尽管已知它能调节其他细菌的生物膜形成和毒力。在这里，我们表明对自己产生的AI-2的趋化性可以介导大肠杆菌的集体行为--自我聚集。自聚集需要运动性，并且在生理细胞密度下对AI-2的趋化作用强烈增强。无论特定生长条件下的细胞间相互作用是由主要的大肠杆菌粘附素(抗原43)还是卷曲纤维介导的，这些效应都是可以观察到的。此外，依赖于AI-2的自聚集增强了细菌的抗逆性，促进了生物膜的形成。一个小分子(自动诱导物2，或AI-2)调节几种细菌的生物膜形成和毒力，但它在大肠杆菌中的作用尚不清楚。在这里，Laganenka等人。结果表明，对自身产生的AI-2的趋化作用介导了大肠杆菌的自我聚集，并促进了对应激的抗性和生物膜的形成。
Bacteria communicate by producing and sensing extracellular signal molecules called autoinducers. Such intercellular signalling, known as quorum sensing, allows bacteria to coordinate and synchronize behavioural responses at high cell densities. Autoinducer 2 (AI-2) is the only known quorum-sensing molecule produced by Escherichia coli but its physiological role remains elusive, although it is known to regulate biofilm formation and virulence in other bacterial species. Here we show that chemotaxis towards self-produced AI-2 can mediate collective behaviour—autoaggregation—of E. coli. Autoaggregation requires motility and is strongly enhanced by chemotaxis to AI-2 at physiological cell densities. These effects are observed regardless whether cell–cell interactions under particular growth conditions are mediated by the major E. coli adhesin (antigen 43) or by curli fibres. Furthermore, AI-2-dependent autoaggregation enhances bacterial stress resistance and promotes biofilm formation. A small molecule (autoinducer 2, or AI-2) regulates biofilm formation and virulence in several bacteria, but its role in Escherichia coli is unknown. Here, Laganenka et al. show that chemotaxis towards self-produced AI-2 mediates autoaggregation and promotes stress resistance and biofilm formation in E. coli.
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影响因子：
3.2
作者：
Bible, Amber;Russell, Matthew H.;Alexandre, Gladys
通讯作者：
Alexandre, Gladys
影响因子：
3.5
作者：
CHEREPANOV, PP;WACKERNAGEL, W
通讯作者：
WACKERNAGEL, W
影响因子：
2.1
作者：
Genevaux, P;Muller, S;Bauda, P
通讯作者：
Bauda, P
影响因子：
3.6
作者：
Danese, PN;Pratt, LA;Kolter, R
通讯作者：
Kolter, R
DOI：
10.1073/pnas.120163297
发表时间：
2000-06-06
影响因子：
11.1
作者：
Datsenko, KA;Wanner, BL
通讯作者：
Wanner, BL