Centre for Bacterial Cell Biology, Biosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
Department of Biochemistry, University of Oxford, Oxford, UK.
Sci Rep. 2020 Oct 21;10(1):17910. doi: 10.1038/s41598-020-74609-5.
The peptidoglycan layer is responsible for maintaining bacterial cell shape and permitting cell division. Cell wall growth is facilitated by peptidoglycan synthases and hydrolases and is potentially modulated by components of the central carbon metabolism. In Bacillus subtilis, UgtP synthesises the glucolipid precursor for lipoteichoic acid and has been suggested to function as a metabolic sensor governing cell size. Here we show that ugtP mutant cells have increased levels of cell wall precursors and changes in their peptidoglycan that suggest elevated DL-endopeptidase activity. The additional deletion of lytE, encoding a DL-endopeptidase important for cell elongation, in the ugtP mutant background produced cells with severe shape defects. Interestingly, the ugtP lytE mutant recovered normal rod-shape by acquiring mutations that decreased the expression of the peptidoglycan synthase PBP1. Together our results suggest that cells lacking ugtP must re-adjust the balance between peptidoglycan synthesis and hydrolysis to maintain proper cell morphology.
肽聚糖层负责维持细菌细胞的形状并允许细胞分裂。肽聚糖合成酶和水解酶促进细胞壁生长，并且中央碳代谢的成分可能对其进行调节。在枯草芽孢杆菌中，UgtP 合成脂磷壁酸的糖脂前体，并且被认为作为代谢传感器来控制细胞大小。在这里，我们表明 ugtP 突变体细胞具有增加的细胞壁前体水平和其肽聚糖的变化，这表明 DL-内肽酶活性升高。在 ugtP 突变体背景中额外缺失编码对于细胞伸长重要的 DL-内肽酶的 lytE，会产生具有严重形状缺陷的细胞。有趣的是，ugtP lytE 突变体通过获得降低肽聚糖合成酶 PBP1 表达的突变恢复了正常的杆状形状。总之，我们的结果表明，缺乏 ugtP 的细胞必须重新调整肽聚糖合成和水解之间的平衡，以维持适当的细胞形态。
