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首页> 外文期刊>Journal of bacteriology >Listeria monocytogenes Multidrug Resistance Transporters and Cyclic Di-AMP, Which Contribute to Type I Interferon Induction, Play a Role in Cell Wall Stress
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Listeria monocytogenes Multidrug Resistance Transporters and Cyclic Di-AMP, Which Contribute to Type I Interferon Induction, Play a Role in Cell Wall Stress

机译：单核细胞增生李斯特菌多药抗性转运蛋白和环状Di-AMP，可促进I型干扰素诱导，在细胞壁应激中发挥作用

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The intracellular bacterial pathogen Listeria monocytogenes activates a robust type I interferon response upon infection. This response is partially dependent on the multidrug resistance (MDR) transporter MdrM and relies on cyclic-di-AMP (c-di-AMP) secretion, yet the functions of MdrM and cyclic-di-AMP that lead to this response are unknown. Here we report that it is not MdrM alone but a cohort of MDR transporters that together contribute to type I interferon induction during infection. In a search for a physiological function of these transporters, we revealed that they play a role in cell wall stress responses. A mutant with deletion of four transporter genes (ΔmdrMTAC) was found to be sensitive to sublethal concentrations of vancomycin due to an inability to produce and shed peptidoglycan under this stress. Remarkably, c-di-AMP is involved in this phenotype, as overexpression of the c-di-AMP phosphodiesterase (PdeA) resulted in increased susceptibility of the ΔmdrMTAC mutant to vancomycin, whereas overexpression of the c-di-AMP diadenylate cyclase (DacA) reduced susceptibility to this drug. These observations suggest a physiological association between c-di-AMP and the MDR transporters and support the model that MDR transporters mediate c-di-AMP secretion to regulate peptidoglycan synthesis in response to cell wall stress.
机译：细胞内细菌病原体单核细胞增生李斯特氏菌在感染后会激活强烈的I型干扰素反应。该反应部分取决于多药抗性（MDR）转运蛋白MdrM，并依赖于环二AMP（c-di-AMP）分泌，但是导致该反应的MdrM和环二AMP的功能尚不清楚。在这里，我们报道了并非仅MdrM，而是一群MDR转运蛋白共同在感染过程中促成了I型干扰素的诱导。在寻找这些转运蛋白的生理功能时，我们发现它们在细胞壁应激反应中起作用。发现具有四个转运蛋白基因（Δ mdrMTAC ）缺失的突变体对亚致命浓度的万古霉素敏感，因为在这种胁迫下无法产生和释放肽聚糖。值得注意的是，c-di-AMP参与了该表型，因为c-di-AMP磷酸二酯酶（PdeA）的过度表达导致Δ mdrMTAC 突变体对万古霉素的敏感性增加，而c-di-AMP的过度表达-di-AMP二腺苷酸环化酶（DacA）降低了对该药物的敏感性。这些观察结果表明c-di-AMP和MDR转运蛋白之间的生理联系，并支持MDR转运蛋白介导c-di-AMP分泌以响应细胞壁应激而调节肽聚糖合成的模型。

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