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多应激反应对大肠杆菌磷脂合成的 dgkA 和 plsB 基因的拮抗调节。

Antagonistic regulation of dgkA and plsB genes of phospholipid synthesis by multiple stress responses in Escherichia coli.

机构信息

LISM, CNRS, Aix-Marseille University, 31 chemin Joseph Aiguier, 13402 Marseille Cedex 20, France.

出版信息

Mol Microbiol. 2011 Jun;80(5):1260-75. doi: 10.1111/j.1365-2958.2011.07641.x. Epub 2011 Apr 5.

Abstract

Phospholipid homeostasis of the bacterial membrane is maintained by biochemical regulation of the synthesis enzymes depending on the environment. However, genes encoding phospholipid synthesis enzymes might also be regulated during stress responses, in order for the bacteria to adapt their growth to changing environments. While few studies have addressed this question, global analyses show that specific genes are activated by alternative Sigma factors, and that phospholipid synthesis genes are co-ordinately regulated during stringent response. In Escherichia coli, the genes coding for glycerol-3-phosphate acyltransferase and diacylglycerol kinase (plsB and dgkA) are found next to each other in divergent orientations, suggesting a co-ordinated regulation. We investigated their regulation and found that these two genes are inversely regulated by a diversity of stress responses. plsB activation by σE is concomitant with a reduced DgkA amount. A second proximal promoter for plsB expression is responsible for basal plsB expression and is inhibited during stringent response. Finally, dgkA is activated by the two-component regulator BasR, linking dgkA function of phospholipid recycling to LPS modifications. In E. coli, PlsB and DgkA are key enzymes in the phospholipid synthesis pathway. Our results show that their expression is a crucial point of integration for different stress signals.

摘要

细菌膜的磷脂稳态是通过生化调节合成酶来维持的,这取决于环境。然而,在应激反应中,编码磷脂合成酶的基因也可能受到调节,以使细菌能够适应不断变化的环境而生长。虽然很少有研究涉及这个问题,但全局分析表明,特定基因被替代 Sigma 因子激活,并且在严格响应期间磷脂合成基因被协调调节。在大肠杆菌中,编码甘油-3-磷酸酰基转移酶和二酰基甘油激酶(plsB 和 dgkA)的基因以不同的方向彼此相邻排列,表明它们受到协调调节。我们研究了它们的调节机制,发现这两个基因受到多种应激反应的反向调节。σE 对 plsB 的激活伴随着 DgkA 数量的减少。plsB 表达的第二个近端启动子负责基础 plsB 表达,并在严格响应期间受到抑制。最后,二组分调节因子 BasR 激活 dgkA,将 dgkA 的磷脂回收功能与 LPS 修饰联系起来。在大肠杆菌中,PlsB 和 DgkA 是磷脂合成途径中的关键酶。我们的研究结果表明,它们的表达是整合不同应激信号的关键点。

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