Enzyme 1 of the phosphoenolpyruvate:sugar phosphotransferase system is involved in resistance to MreB disruption in wild-type and ∆envC cells.
Enzyme 1 of the phosphoenolpyruvate:sugar phosphotransferase system is involved in resistance to MreB disruption in wild-type and ∆envC cells.
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DOI：
10.1111/mmi.14988
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发表时间：
2022-11
影响因子：
3.6
通讯作者：
Morgenstein, Randy M.
中科院分区：
文献类型：
--
作者：
Sloan, Ryan;Surber, Jacob;Roy, Emma J.;Hartig, Ethan;Morgenstein, Randy M.
细菌细胞壁的合成是由两种蛋白质复合物决定的：长体和分裂体。长体由肌动蛋白同源物MreB协调，而分体由微管蛋白同源物FtsZ组织。虽然这两个系统必须相互协调，以确保延伸和分裂是共同调节的，但这种串扰尚未得到充分研究。使用MreB解聚剂A22，我们发现多个基因缺失导致细胞对MreB解聚的敏感性增加。其中一个基因编码EnvC， EnvC是分裂体的一部分，在细胞质分裂完成后，通过激活特定的酰胺酶，负责分裂子细胞。在这里，我们发现这种对A22的敏感性增加通过两个已知的EnvC的酰胺酶靶点：AmiA和AmiB起作用。此外，抑制因子分析显示，磷酸烯醇丙酮酸：糖磷酸转移酶系统（PTS）的酶1突变可以抑制A22在野生型和envC缺失细胞中的作用。这些工作有助于将延伸、分裂和代谢联系起来。ΔenvC细胞对MreB靶向抗生素A22更敏感。抑制因子分析显示，磷酸烯醇丙酮酸：糖磷酸转移酶系统的1号酶（ptsI）缺失能够抑制野生型和ΔenvC细胞中由A22处理引起的生长缺陷。此外，ptsI的缺失导致两种背景下的小细胞表型。细菌的细胞形状是由细胞壁决定的。细胞壁由两个系统构建：由MreB协调的长体和由FtsZ协调的分裂体。这两个系统必须相互协调以保持细胞的完整性。在这里，我们展示了分裂蛋白EnvC的缺失，导致细长和连锁的细胞对MreB解聚药物A22更敏感。这种敏感性通过EnvC: AmiA和AmiB的靶标起作用。我们发现磷酸烯醇丙酮酸：糖磷酸转移酶系统的酶1的缺失能够在envC缺失中降低细胞大小和A22敏感性。
Cell wall synthesis in bacteria is determine by two protein complexes: the elongasome and divisome. The elongasome is coordinated by the actin homolog MreB while the divisome is organized by the tubulin homolog FtsZ. While these two systems must coordinate with each other to ensure that elongation and division are coregulated, this cross talk has been understudied. Using the MreB depolymerizing agent, A22, we found that multiple gene deletions result in cells exhibiting increased sensitivity to MreB depolymerization. One of those genes encodes for EnvC, a part of the divisome that is responsible for splitting daughter cells after the completion of cytokinesis through the activation of specific amidases. Here we show this increased sensitivity to A22 works through two known amidase targets of EnvC: AmiA and AmiB. In addition, suppressor analysis revealed that mutations in enzyme 1 of the phosphoenolpyruvate:sugar phosphotransferase system (PTS) can suppress the effects of A22 in both wild-type and envC deletion cells. Together this work helps to link elongation, division, and metabolism. ΔenvC cells are more sensitive to the MreB targeting antibiotic A22. Suppressor analysis revealed that deletion of enzyme 1 (ptsI) of the phosphoenolpyruvate:sugar phosphotransferase system is able to suppress the growth defects caused by A22 treatment in both wild-type and ΔenvC cells. Furthermore, deletion of ptsI results in a small cell phenotype in both backgrounds. Bacterial cell shape is determined by its cell wall. The cell wall is built using two systems: the elongasome, coordinated by MreB and divisome, coordinated by FtsZ. These two systems must coordinate with each other to maintain cell integrity. Here we show that deletion of a divisome protein, EnvC, results in elongated and chained cells that are more sensitive to the MreB depolymerizing drug A22. This sensitivity works through the targets of EnvC: AmiA and AmiB. We found that deletion of enzyme 1 of the phosphoenolpyruvate:sugar phosphotransferase system is able to reduce both cell size and A22 sensitivity in an envC deletion.
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影响因子：
4.5
作者：
Govindarajan S;Amster-Choder O
通讯作者：
Amster-Choder O
影响因子：
5.2
作者：
Barton B;Grinnell A;Morgenstein RM
通讯作者：
Morgenstein RM
影响因子：
2.9
作者：
Dimitrova, MN;Szczepanowski, RH;Ginsburg, A
通讯作者：
Ginsburg, A
DOI：
10.1073/pnas.0402638101
发表时间：
2004-06-08
影响因子：
11.1
作者：
Gitai, Z;Dye, N;Shapiro, L
通讯作者：
Shapiro, L
影响因子：
11.4
作者：
Bendezu, Felipe O.;Hale, Cynthia A.;de Boer, Piet A. J.
通讯作者：
de Boer, Piet A. J.