In rod-shaped Gram-negative bacteria, penicillin binding protein 1a (PBP1a) and 1b (PBP1b) form peptidoglycan-synthesizing complexes with the outer membrane lipoprotein LpoA and LpoB, respectively. Escherichia coli mutants lacking PBP1b/LpoB are sicker than those lacking PBP1a/LpoA. However, we previously found that mutants lacking PBP1a/LpoA but not PBP1b/LpoB are deleterious in Shewanella oneidensis. Here, we show that S. oneidensis PBP1a (SoPBP1a) contains conserved signature motifs with its E. coli counterpart, EcPBP1a. Although EcPBP1a play a less prominent role in E. coli, it is capable of substituting for the SoPBP1a in a manner dependent on SoLpoA. In S. oneidensis, expression of PBP1b is lower than PBP1a, and therefore the additional expression of SoPBP1b at low levels can functionally compensate for the absence of SoPBP1a. Importantly, S. oneidensis PBP1a variants lacking either glycosyltransferase (GTase) or transpeptidase (TPase) activity fail to maintain normal morphology and cell envelope integrity. Similarly, SoPBP1b variants also fail to compensate for the loss of SoPBP1a. Furthermore, overproduction of variants of SoPBP1a, but not SoPBP1b, has detrimental effects on cell morphology in S. oneidensis wild type cells. Overall, our results indicate that the combined enzymatic activities of SoPBP1a are essential for cell wall homeostasis.

中文翻译：

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PBP1a糖基转移酶和转肽酶活性都是维持希瓦氏菌中细胞形态和包膜完整性所必需的。

在杆状革兰氏阴性细菌中，青霉素结合蛋白1a（PBP1a）和1b（PBP1b）分别与外膜脂蛋白LpoA和LpoB形成肽聚糖合成复合物。缺乏PBP1b / LpoB的大肠杆菌突变体比缺乏PBP1a / LpoA的大肠杆菌致病。然而，我们以前发现缺少PBP1a / LpoA而不缺少PBP1b / LpoB的突变体在印度希瓦氏菌中是有害的。在这里，我们显示沙门氏菌PBP1a（SoPBP1a）包含与其大肠杆菌对应物EcPBP1a保守的签名基序。尽管EcPBP1a在大肠杆菌中的作用较小，但它能够以依赖SoLpoA的方式替代SoPBP1a。在沙门氏菌中，PBP1b的表达低于PBP1a，因此，低水平的SoPBP1b的额外表达可以在功能上补偿SoPBP1a的缺失。重要的是，S。缺乏糖基转移酶（GTase）或转肽酶（TPase）活性的oneidensis PBP1a变体无法维持正常的形态和细胞包膜完整性。同样，SoPBP1b变体也无法补偿SoPBP1a的损失。此外，SoPBP1a变体的过量生产，而不是SoPBP1b的过量生产，对oneidensis野生型细胞的细胞形态具有不利影响。总的来说，我们的结果表明，SoPBP1a的组合酶活性对于细胞壁稳态至关重要。对沙门氏菌野生型细胞的细胞形态有不利影响。总的来说，我们的结果表明，SoPBP1a的组合酶活性对于细胞壁稳态至关重要。对沙门氏菌野生型细胞的细胞形态有不利影响。总的来说，我们的结果表明，SoPBP1a的组合酶活性对于细胞壁稳态至关重要。