Reciprocal control between a bacterium's regulatory system and the modification status of its lipopolysaccharide.
Reciprocal control between a bacterium's regulatory system and the modification status of its lipopolysaccharide.
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DOI：
10.1016/j.molcel.2012.07.017
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发表时间：
2012-09-28
期刊：
影响因子：
16
通讯作者：
Groisman, Eduardo A.
中科院分区：
文献类型：
--
作者：
Kato, Akinori;Chen, H. Deborah;Latifi, Tammy;Groisman, Eduardo A.
革兰氏阴性菌通常修饰其脂多糖（LPS），从而增加对抗菌剂的抗性并避免宿主免疫系统。然而，目前尚不清楚细菌如何调节LPS修饰酶的水平和活性，以响应其LPS的修饰状态。我们现在通过研究肠道沙门氏菌中LPS修饰的主要调节因子来解决这个问题。我们报告说，PmrA/PmrB系统控制的膜肽，抑制LpxT，负责增加LPS负电荷的酶的活性的表达。LpxT的抑制和带正电荷的L-4-氨基阿拉伯糖的PmrA依赖性掺入LPS中降低了Fe 3+与细菌细胞的结合。由于Fe 3+是传感器PmrB的活化配体，因此PmrA依赖性LPS修饰基因的转录减少。这种机制使细菌能够通过其对调节细胞表面修饰的系统的诱导信号的可用性的影响来感知它们的细胞表面。
Gram-negative bacteria often modify their lipopolysaccharide (LPS) thereby increasing resistance to antimicrobial agents and avoidance of the host immune system. However, it is unclear how bacteria adjust the levels and activities of LPS-modifying enzymes in response to the modification status of their LPS. We now address this question by investigating the major regulator of LPS modifications in Salmonella enterica. We report that the PmrA/PmrB system controls expression of a membrane peptide that inhibits the activity of LpxT, an enzyme responsible for increasing the LPS negative charge. LpxT’s inhibition and the PmrA-dependent incorporation of positively charged L-4-aminoarabinose into the LPS decrease Fe3+ binding to the bacterial cell. Because Fe3+ is an activating ligand for the sensor PmrB, transcription of PmrA-dependent LPS-modifying genes is reduced. This mechanism enables bacteria to sense their cell surface by its effect on the availability of an inducing signal for the system regulating cell surface modifications.
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