ActS activates peptidoglycan amidases during outer membrane stress in Escherichia coli.
ActS activates peptidoglycan amidases during outer membrane stress in Escherichia coli.
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DOI：
10.1111/mmi.14712
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发表时间：
2021-07
影响因子：
3.6
通讯作者：
Polissi A
中科院分区：
文献类型：
--
作者：
Gurnani Serrano CK;Winkle M;Martorana AM;Biboy J;Morè N;Moynihan P;Banzhaf M;Vollmer W;Polissi A
E.大肠杆菌依赖于合成肽聚糖（PG）和外膜（OM）的多蛋白质机制的协同活动。我们以前的工作发现，脂多糖（LPS）输出到OM的消耗诱导了一个重要的PG重塑过程，涉及LD-转肽酶（LDTs），PBP 1B和羧肽酶PBP 6a的糖基转移酶功能。因此，如果OM生物合成缺陷的细胞缺乏这些PG酶中的任何一种，则它们会裂解。在这里，我们报告了与LPS转运受损的ldtF突变体相关的形态缺陷和溶解，通过预测的OM锚定脂蛋白ActS（以前的YgeR）的丢失而减轻。我们发现ActS是LytM型肽聚糖内肽酶的一个非活性成员，这是由于降解的催化结构域。ActS能够激活所有三种主要的周质肽聚糖酰胺酶AmiA、AmiB和AmiC，这些酶先前报道仅被EnvC和/或NlpD激活。我们的数据还表明，在体内ActS优先激活AmiC，其功能与细胞包膜应力。应激细胞中的ActS活性以某种方式受LdtF控制，导致轻度连锁表型（左图）。ldtF的缺失导致假ActS活化，引起细胞裂解（中心图）。缺乏LdtF的细胞中actS的缺失抑制裂解表型（右图）。在此条件下，AmiC被NlpD充分控制，使其能够部分恢复细胞分离。
The integrity of the cell envelope of E. coli relies on the concerted activity of multi‐protein machineries that synthesize the peptidoglycan (PG) and the outer membrane (OM). Our previous work found that the depletion of lipopolysaccharide (LPS) export to the OM induces an essential PG remodeling process involving LD‐transpeptidases (LDTs), the glycosyltransferase function of PBP1B and the carboxypeptidase PBP6a. Consequently, cells with defective OM biogenesis lyse if they lack any of these PG enzymes. Here we report that the morphological defects, and lysis associated with a ldtF mutant with impaired LPS transport, are alleviated by the loss of the predicted OM‐anchored lipoprotein ActS (formerly YgeR). We show that ActS is an inactive member of LytM‐type peptidoglycan endopeptidases due to a degenerated catalytic domain. ActS is capable of activating all three main periplasmic peptidoglycan amidases, AmiA, AmiB, and AmiC, which were previously reported to be activated only by EnvC and/or NlpD. Our data also suggest that in vivo ActS preferentially activates AmiC and that its function is linked to cell envelope stress. ActS activity in stressed cells is somehow controlled by LdtF resulting in mild chaining phenotype (left panel). Deletion of ldtF leads to spurious ActS activation causing cell lysis (central panel). Deletion of actS in cells lacking LdtF suppresses the lysis phenotype (right panel). At this condition AmiC is sufficiently controlled by NlpD enabling it to partially restore cell separation.
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影响因子：
62.1
作者：
Lundstedt E;Kahne D;Ruiz N
通讯作者：
Ruiz N
DOI：
10.1073/pnas.0805309105
发表时间：
2008-12-09
影响因子：
11.1
作者：
Huang, Kerwyn Casey;Mukhopadhyay, Ranjan;Wingreen, Ned S.
通讯作者：
Wingreen, Ned S.
大肠杆菌K-12的构造框架，单基因敲除突变体：Keio Collection。
影响因子：
9.9
作者：
通讯作者：
--
影响因子：
14.9
作者：
Keseler IM;Collado-Vides J;Santos-Zavaleta A;Peralta-Gil M;Gama-Castro S;Muñiz-Rascado L;Bonavides-Martinez C;Paley S;Krummenacker M;Altman T;Kaipa P;Spaulding A;Pacheco J;Latendresse M;Fulcher C;Sarker M;Shearer AG;Mackie A;Paulsen I;Gunsalus RP;Karp PD
通讯作者：
Karp PD
DOI：
10.1073/pnas.120163297
发表时间：
2000-06-06
影响因子：
11.1
作者：
Datsenko, KA;Wanner, BL
通讯作者：
Wanner, BL