細菌如何響應外界刺激，實現我保護？

Gene expression kinetics governs stimulus-specific decoration of theSalmonellaouter membrane

【遇見·按】本文報道了沙門氏菌在低鎂離子與弱酸性pH時激活PmrA從而產生不同類型脂質A的機制。

Model for activation of the PhoP/PhoQ and PmrA/PmrB two-component systems and regulation by the PhoP and PmrA proteins.

【背景】脂質A(Lipid A)位於革蘭氏陰性菌外膜的脂多糖(LPS)分子的內部；Lipid A能被宿主免疫系統識別並為陽離子型抗菌化合物所靶向；在沙門氏菌中，轉錄調控因子PmrA可促進Lipid A的磷酸化修飾，這些修飾可降低LPS的負電性從而增加宿主對陽離子型多肽抗生素多粘菌素B(多粘菌素B)的抗性；

【內容】本文報道了低鎂離子與弱酸性pH激活PmrA時沙門氏菌產生不同脂質A譜的機制。低Mg 2+可激活調節蛋白PhoP，使得磷酸化Lipid A與4-氨基-4-脫氧-1-氨基阿拉伯糖(4-amino-4-deoxy-l-aminoarabinose, L-Ara4N)反應。相比之下，弱酸性pH有利於用L-Ara4N和磷酸乙醇胺(pEtN)的混合物與磷酸化Lipid A反應。儘管L-Ara4N比pEtN更多地減少LPS負電荷，但僅用L-Ara4N修飾磷酸化Lipid A需要先瞬時增加Lipid A負電荷。本文結果表明細菌是如何針對不同的壓力調整其細胞表面結構。

Schematic of the lipid A structure over time after bacteria encounter low Mg2+ or a mildly acidic pH.Under low Mg2+, lpxT is activated by PhoP within 5 min, resulting in 1-PP lipid A. The additional phosphate group at the 1-phosphate prevents the addition of pEtN at this position. By 30 min, lipid A is preferentially modified at the 4′-phosphate with L-Ara4N. PmrR later inhibits LpxT, thereby preventing the incorporation of a phosphate at the 1 position. pEtN is not detected at later times despite inhibition of LpxT by PmrR, suggesting that L-Ara4N–modified lipid A is not a good substrate for PmrC. In a mildly acidic pH, transcription of lpxT gene occurs after that of genes encoding Ugd, PbgP, PmrC, and PmrR, resulting in lipid A modified with both L-Ara4N and pEtN.

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