Where antibiotic resistance mutations meet quorum-sensing.
Where antibiotic resistance mutations meet quorum-sensing.
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DOI：
10.15698/mic2014.07.158
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发表时间：
2014-06-25
期刊：
影响因子：
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通讯作者：
Knight CG
中科院分区：
文献类型：
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作者：
Krašovec R;Belavkin RV;Aston JA;Channon A;Aston E;Rash BM;Kadirvel M;Forbes S;Knight CG
我们不需要重复抗生素耐药微生物在全球崛起的可怕故事。但是，如果有可能通过从头突变来控制抗生素耐药性的发展速度呢？有些细菌似乎已经做到了这一点：它们根据自身的生物环境，调整自身的变异速率，使其对抗生素产生耐药性。在我们最近的研究[Krašovec， et al.]Commun Nat。（2014）， 5,3742]我们发现这种修饰取决于细菌种群的密度和细胞间的相互作用（而不是，例如，压力水平）。具体来说，我们使用的野生型大肠杆菌菌株将在最低葡萄糖培养基中根据野生型细胞的密度改变其对利福平抗性的突变率。有趣的是，密度越高，突变率越低（图1）。为什么这种新型的密度依赖性“突变率可塑性”（DD-MRP）会发生，这在几个层面上是一个问题。答案目前不完整，但涉及群体感应基因luxS及其在活化甲基循环中的作用。
We do not need to rehearse the grim story of the global rise of antibiotic resistant microbes. But what if it were possible to control the rate with which antibiotic resistance evolves by de novo mutation? It seems that some bacteria may already do exactly that: they modify the rate at which they mutate to antibiotic resistance dependent on their biological environment. In our recent study [Krašovec, et al. Nat. Commun. (2014), 5, 3742] we find that this modification depends on the density of the bacterial population and cell-cell interactions (rather than, for instance, the level of stress). Specifically, the wild-type strains of Escherichia coli we used will, in minimal glucose media, modify their rate of mutation to rifampicin resistance according to the density of wild-type cells. Intriguingly, the higher the density, the lower the mutation rate (Figure 1). Why this novel density-dependent ‘mutation rate plasticity’ (DD-MRP) occurs is a question at several levels. Answers are currently fragmentary, but involve the quorum-sensing gene luxS and its role in the activated methyl cycle.