Cell division is antagonized by the activity of peptidoglycan endopeptidases that promote cell elongation.,Molecular Microbiology

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Cell division is antagonized by the activity of peptidoglycan endopeptidases that promote cell elongation.
Molecular Microbiology ( IF 2.6 ) Pub Date : 2020-08-31 , DOI: 10.1111/mmi.14587
Thao T Truong ₁ , Andrea Vettiger ₁ , Thomas G Bernhardt _{1,

2}

Affiliation

A peptidoglycan (PG) cell wall composed of glycans crosslinked by short peptides surrounds most bacteria and protects them against osmotic rupture. In Escherichia coli, cell elongation requires crosslink cleavage by PG endopeptidases to make space for the incorporation of new PG material throughout the cell cylinder. Cell division, on the contrary, requires the localized synthesis and remodeling of new PG at midcell by the divisome. Little is known about the factors that modulate transitions between these two modes of PG biogenesis. In a transposon‐insertion sequencing screen to identify mutants synthetically lethal with a defect in the division protein FtsP, we discovered that mutants impaired for cell division are sensitive to elevated activity of the endopeptidases. Increased endopeptidase activity in these cells was shown to interfere with the assembly of mature divisomes, and conversely, inactivation of MepS was found to suppress the lethality of mutations in essential division genes. Overall, our results are consistent with a model in which the cell elongation and division systems are in competition with one another and that control of PG endopeptidase activity represents an important point of regulation influencing the transition from elongation to the division mode of PG biogenesis.

中文翻译：

促进细胞伸长的肽聚糖内肽酶的活性拮抗细胞分裂。

由短肽交联的聚糖组成的肽聚糖 (PG) 细胞壁包围着大多数细菌并保护它们免受渗透破裂。在大肠杆菌中，细胞伸长需要 PG 内肽酶进行交联裂解，以便为在整个细胞圆柱体中掺入新的 PG 材料腾出空间。相反，细胞分裂需要分裂体在中间细胞中局部合成和重塑新的 PG。关于调节这两种 PG 生物发生模式之间转换的因素知之甚少。在用于识别具有分裂蛋白 FtsP 缺陷的合成致死突变体的转座子插入测序筛选中，我们发现细胞分裂受损的突变体对内肽酶活性升高很敏感。这些细胞中增加的内肽酶活性被证明会干扰成熟分裂体的组装，相反，发现 MepS 的失活会抑制基本分裂基因突变的致死率。总体，

更新日期：2020-08-31

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