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首页> 外文期刊>Genes & Genetic Systems >The Bacillus subtilis essential gene dgkB is dispensable in mutants with defective lipoteichoic acid synthesis
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The Bacillus subtilis essential gene dgkB is dispensable in mutants with defective lipoteichoic acid synthesis

机译:枯草芽孢杆菌必不可少的基因dgkB可用于脂联蛋白酸合成缺陷的突变体中

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References(33) Cited-By(8) The dgkB gene is essential for the growth of Bacillus subtilis. It encodes a diacylglycerol (DG) kinase that converts DG to phosphatidic acid to reintroduce it into the phospholipid synthesis pathway. Repression of the dgkB gene placed under a regulatable promoter causes accumulation of DG and leads to lethality. DG is formed as a byproduct of the synthesis of lipoteichoic acid (LTA), a polyanionic component of the cell envelope. B. subtilis synthesizes LTA by polymerizing the glycerophosphate moiety of phosphatidylglycerol (PG) onto a glucolipid membrane anchor, and releasing the DG moiety of PG. B. subtilis has four genes homologous to Staphylococcus aureus ltaS, which encodes LTA synthase. Disruption of either or both of two genes, yflE and yfnI, whose products show higher homology with S. aureus LtaS among the four homologues, suppressed the lethality caused by dgkB repression. In cells with dgkB repression, DG was accumulated to 43 ± 3% of total lipids, about three times the content of wild type cells (13 ± 1%). Disruption of yfnI in the dgkB-repressed cells reduced the DG content to 15 ± 2%, but yflE-disruption did not (42 ± 1%); this was probably due to efficient LTA synthesis by YfnI in the yflE-disrupted cells. Further introduction of a disrupted allele of ugtP, encoding glucolipid synthase that consumes DG as a substrate, partially lowered the colony forming capacity in strains with yflE-disruption. A disrupted dgkB allele was successfully introduced into strains disrupted for either or both of yflE and yfnI, indicating that the essential gene dgkB is dispensable in mutants defective in LTA synthesis.
机译:参考文献(33)被引用的By(8)dgkB基因对于枯草芽孢杆菌的生长至关重要。它编码一种二酰基甘油(DG)激酶,该激酶可将DG转化为磷脂酸,从而将其重新引入磷脂合成途径。抑制可调节启动子下的dgkB基因会导致DG积累并导致致死性。 DG是脂环磷酸(LTA)合成的副产物,脂环磷酸是细胞膜的聚阴离子成分。枯草芽孢杆菌通过将磷脂酰甘油(PG)的甘油磷酸酯部分聚合到糖脂膜锚上并释放PG的DG部分来合成LTA。枯草芽孢杆菌具有四个与金黄色葡萄球菌ltaS同源的基因,该基因编码LTA合酶。 yflE和yfnI这两个基因之一或两者的破坏,在四个同源物中与金黄色葡萄球菌LtaS的同源性更高,抑制了dgkB抑制所致的致死性。在具有dgkB抑制作用的细胞中,DG积累至总脂质的43±3%,约为野生型细胞含量(13±1%)的三倍。 dgkB抑制的细胞中yfnI的破坏使DG含量降低至15±2%,而yflE破坏则没有(42±1%)。这可能是由于YfnI干扰了yflE的细胞有效合成了LTA。进一步引入编码以DG为底物的糖脂合酶的ugtP破坏等位基因,部分降低了yflE破坏菌株的菌落形成能力。 dgkB等位基因被成功地导入了被yflE和yfnI之一或两者破坏的菌株,这表明必需基因dgkB在LTA合成缺陷的突变体中是可有可无的。

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