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The Essential UPP Phosphatase Pair BcrC and UppP Connects Cell Wall Homeostasis during Growth and Sporulation with Cell Envelope Stress Response in Bacillus subtilis.
Frontiers in Microbiology ( IF 4.0 ) Pub Date : 2017-12-21 , DOI: 10.3389/fmicb.2017.02403
Jara Radeck 1 , Nina Lautenschläger 1 , Thorsten Mascher 1
Frontiers in Microbiology ( IF 4.0 ) Pub Date : 2017-12-21 , DOI: 10.3389/fmicb.2017.02403
Jara Radeck 1 , Nina Lautenschläger 1 , Thorsten Mascher 1
Affiliation
The bacterial cell wall separates the cell from its surrounding and protects it from environmental stressors. Its integrity is maintained by a highly regulated process of cell wall biosynthesis. The membrane-located lipid II cycle provides cell wall building blocks that are assembled inside the cytoplasm to the outside for incorporation. Its carrier molecule, undecaprenyl phosphate (UP), is then recycled by dephosphorylation from undecaprenyl pyrophosphate (UPP). In Bacillus subtilis, this indispensable reaction is catalyzed by the UPP phosphatases BcrC and UppP. Here, we study the physiological function of both phosphatases with respect to morphology, cell wall homeostasis and the resulting cell envelope stress response (CESR). We demonstrate that uppP and bcrC represent a synthetic lethal gene pair, which encodes an essential physiological function. Accordingly, cell growth and morphology were severely impaired during exponential growth if the overall UPP phosphatase level was limiting. UppP, but not BcrC, was crucial for normal sporulation. Expression of bcrC, but not uppP, was upregulated in the presence of cell envelope stress conditions caused by bacitracin if UPP phosphatase levels were limited. This homeostatic feedback renders BcrC more important during growth than UppP, particularly in defense against cell envelope stress.
中文翻译:
必需的UPP磷酸酶对BcrC和UppP在枯草芽孢杆菌的生长和孢子形成过程中通过细胞包膜应力反应连接细胞壁稳态。
细菌细胞壁将细胞与其周围环境隔离开来,并使其免受环境压力。它的完整性通过细胞壁生物合成的高度调控过程得以维持。位于膜上的脂质II循环提供了细胞壁构件,这些构件在细胞质内部组装到外部以进行整合。然后将其载体分子,十一碳烯基磷酸酯(UP),通过十一碳烯基焦磷酸酯(UPP)中的去磷酸化作用进行再循环。在枯草芽孢杆菌中,该不可缺少的反应由UPP磷酸酶BcrC和UppP催化。在这里,我们研究了两种磷酸酶在形态,细胞壁稳态和所产生的细胞包膜应激反应(CESR)方面的生理功能。我们证明了uppP和bcrC代表合成的致死基因对,编码基本的生理功能。因此,如果总体UPP磷酸酶水平受到限制,则在指数生长过程中会严重损害细胞生长和形态。UppP(而非BcrC)对于正常的孢子形成至关重要。如果UPP磷酸酶水平受到限制,则在由杆菌肽引起的细胞包膜应激条件下,bcrC的表达而非uppP的表达上调。这种稳态反馈使BcrC在生长过程中比UppP更重要,特别是在防御细胞膜应力方面。如果UPP磷酸酶水平受到限制,则在由杆菌肽引起的细胞包膜应激条件下,其上调被上调。这种稳态反馈使BcrC在生长过程中比UppP更重要,特别是在防御细胞膜应力方面。如果UPP磷酸酶水平受到限制,则在由杆菌肽引起的细胞包膜应激条件下,其上调被上调。这种稳态反馈使BcrC在生长过程中比UppP更重要,特别是在防御细胞膜应力方面。
更新日期:2019-11-01
中文翻译:
![](https://scdn.x-mol.com/jcss/images/paperTranslation.png)
必需的UPP磷酸酶对BcrC和UppP在枯草芽孢杆菌的生长和孢子形成过程中通过细胞包膜应力反应连接细胞壁稳态。
细菌细胞壁将细胞与其周围环境隔离开来,并使其免受环境压力。它的完整性通过细胞壁生物合成的高度调控过程得以维持。位于膜上的脂质II循环提供了细胞壁构件,这些构件在细胞质内部组装到外部以进行整合。然后将其载体分子,十一碳烯基磷酸酯(UP),通过十一碳烯基焦磷酸酯(UPP)中的去磷酸化作用进行再循环。在枯草芽孢杆菌中,该不可缺少的反应由UPP磷酸酶BcrC和UppP催化。在这里,我们研究了两种磷酸酶在形态,细胞壁稳态和所产生的细胞包膜应激反应(CESR)方面的生理功能。我们证明了uppP和bcrC代表合成的致死基因对,编码基本的生理功能。因此,如果总体UPP磷酸酶水平受到限制,则在指数生长过程中会严重损害细胞生长和形态。UppP(而非BcrC)对于正常的孢子形成至关重要。如果UPP磷酸酶水平受到限制,则在由杆菌肽引起的细胞包膜应激条件下,bcrC的表达而非uppP的表达上调。这种稳态反馈使BcrC在生长过程中比UppP更重要,特别是在防御细胞膜应力方面。如果UPP磷酸酶水平受到限制,则在由杆菌肽引起的细胞包膜应激条件下,其上调被上调。这种稳态反馈使BcrC在生长过程中比UppP更重要,特别是在防御细胞膜应力方面。如果UPP磷酸酶水平受到限制,则在由杆菌肽引起的细胞包膜应激条件下,其上调被上调。这种稳态反馈使BcrC在生长过程中比UppP更重要,特别是在防御细胞膜应力方面。