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鉴定隔膜肽聚糖聚合酶 FtsW 的潜在活性位点。

Identification of the potential active site of the septal peptidoglycan polymerase FtsW.

机构信息

Department of Microbiology, Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, Hubei, China.

InBioS-Centre d'Ingénierie des Protéines, Liège University, Liège, Belgium.

出版信息

PLoS Genet. 2022 Jan 5;18(1):e1009993. doi: 10.1371/journal.pgen.1009993. eCollection 2022 Jan.

Abstract

SEDS (Shape, Elongation, Division and Sporulation) proteins are widely conserved peptidoglycan (PG) glycosyltransferases that form complexes with class B penicillin-binding proteins (bPBPs, with transpeptidase activity) to synthesize PG during bacterial cell growth and division. Because of their crucial roles in bacterial morphogenesis, SEDS proteins are one of the most promising targets for the development of new antibiotics. However, how SEDS proteins recognize their substrate lipid II, the building block of the PG layer, and polymerize it into glycan strands is still not clear. In this study, we isolated and characterized dominant-negative alleles of FtsW, a SEDS protein critical for septal PG synthesis during bacterial cytokinesis. Interestingly, most of the dominant-negative FtsW mutations reside in extracellular loops that are highly conserved in the SEDS family. Moreover, these mutations are scattered around a central cavity in a modeled FtsW structure, which has been proposed to be the active site of SEDS proteins. Consistent with this, we found that these mutations blocked septal PG synthesis but did not affect FtsW localization to the division site, interaction with its partners nor its substrate lipid II. Taken together, these results suggest that the residues corresponding to the dominant-negative mutations likely constitute the active site of FtsW, which may aid in the design of FtsW inhibitors.

摘要

SED 蛋白(形状、伸长、分裂和孢子形成)是广泛保守的肽聚糖(PG)糖基转移酶,它们与 B 类青霉素结合蛋白(具有转肽酶活性的 bPBPs)形成复合物,在细菌细胞生长和分裂过程中合成 PG。由于它们在细菌形态发生中的关键作用,SED 蛋白是开发新抗生素的最有前途的目标之一。然而,SED 蛋白如何识别其底物脂质 II,即 PG 层的构建块,并将其聚合成长聚糖链仍不清楚。在这项研究中,我们分离并鉴定了 FtsW 的显性负突变体,FtsW 是细菌胞质分裂过程中隔膜 PG 合成所必需的 SEDS 蛋白。有趣的是,大多数显性负 FtsW 突变位于 SEDS 家族中高度保守的细胞外环中。此外,这些突变分散在模型化的 FtsW 结构的中央腔周围,该结构被提议为 SEDS 蛋白的活性位点。与这一观点一致,我们发现这些突变阻断了隔膜 PG 的合成,但不影响 FtsW 定位到分裂部位、与伴侣的相互作用或其底物脂质 II。总之,这些结果表明,对应于显性负突变的残基可能构成了 FtsW 的活性位点,这可能有助于设计 FtsW 抑制剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f018/8765783/042ff4eb50b8/pgen.1009993.g001.jpg

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