Hernández-Rocamora Víctor M, Martorana Alessandra M, Belloso Aitana, Ballesteros Daniel, Zaccaria Marta, Perez Amilcar J, Iorga Bogdan I, Abia David, Gray Joe, Breukink Eefjan, Xiao Jie, Pazos Manuel, Polissi Alessandra, Vollmer Waldemar
Centre for Bacterial Cell Biology, Biosciences Institute, Newcastle University, Newcastle upon Tyne, United Kingdom.
Department of Pharmacological and Biomolecular Sciences "Rodolfo Paoletti", University of Milano, Milano, Italy.
PLoS Genet. 2025 Sep 5;21(9):e1011626. doi: 10.1371/journal.pgen.1011626. eCollection 2025 Sep.
Peptidoglycan hydrolases facilitate bacterial cell wall growth by creating space for insertion of new material and allowing physical separation of daughter cells. In Escherichia coli, three peptidoglycan amidases, AmiA, AmiB and AmiC, cleave septal peptidoglycan during cell division. The LytM-domain proteins EnvC, NlpD and ActS activate these amidases either from inside the cell or the outer membrane: EnvC binds to the cytoplasmic membrane-anchored divisome components FtsEX, while NlpD and ActS are outer membrane-anchored lipoproteins. Here we report the identification of a novel periplasmic deacetylase called SddA that removes acetyl groups from denuded peptidoglycan glycan strands, the products of amidases. The sddA gene is co-expressed with the gene encoding EnvC, linking SddA function to amidase activation. Consistent with this link, the deletion of sddA alleviates phenotypes associated with lack of amidase activation, while overexpression of sddA alleviates phenotypes related to a defective Tol-Pal system and causes cell chaining due to reduced septum peptidoglycan cleavage. We present a model according to which SddA modulates the activation of the septum-splitting amidases during cell division.
肽聚糖水解酶通过为插入新物质创造空间并使子细胞物理分离来促进细菌细胞壁生长。在大肠杆菌中，三种肽聚糖酰胺酶AmiA、AmiB和AmiC在细胞分裂过程中切割隔膜肽聚糖。LytM结构域蛋白EnvC、NlpD和ActS从细胞内部或外膜激活这些酰胺酶：EnvC与细胞质膜锚定的分裂体成分FtsEX结合，而NlpD和ActS是外膜锚定的脂蛋白。在这里，我们报告鉴定了一种名为SddA的新型周质脱乙酰酶，它从酰胺酶产物——裸露的肽聚糖聚糖链上去除乙酰基。sddA基因与编码EnvC的基因共表达，将SddA的功能与酰胺酶激活联系起来。与此联系一致，sddA的缺失减轻了与酰胺酶激活缺乏相关的表型，而sddA的过表达减轻了与Tol-Pal系统缺陷相关的表型，并由于隔膜肽聚糖切割减少而导致细胞成链。我们提出了一个模型，根据该模型，SddA在细胞分裂过程中调节隔膜分裂酰胺酶的激活。
