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Z 环膜锚与细胞壁合成酶结合,启动细菌细胞分裂。

Z-ring membrane anchors associate with cell wall synthases to initiate bacterial cell division.

机构信息

Centre for Bacterial Cell Biology, Institute for Cell and Molecular Biosciences, Newcastle University, Richardson Road, Newcastle upon Tyne, NE2 4AX, UK.

Centro Nacional de Biotecnología-Consejo Superior de Investigaciones Científicas (CNB-CSIC), Darwin 3, 28049, Madrid, Spain.

出版信息

Nat Commun. 2018 Nov 30;9(1):5090. doi: 10.1038/s41467-018-07559-2.

DOI:10.1038/s41467-018-07559-2
PMID:30504892
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6269477/
Abstract

During the transition from elongation to septation, Escherichia coli establishes a ring-like peptidoglycan growth zone at the future division site. This preseptal peptidoglycan synthesis does not require the cell division-specific peptidoglycan transpeptidase PBP3 or most of the other cell division proteins, but it does require FtsZ, its membrane-anchor ZipA and at least one of the bi-functional transglycosylase-transpeptidases, PBP1A or PBP1B. Here we show that PBP1A and PBP1B interact with ZipA and localise to preseptal sites in cells with inhibited PBP3. ZipA stimulates the glycosyltransferase activity of PBP1A. The membrane-anchored cell division protein FtsN localises at preseptal sites and stimulates both activities of PBP1B. Genes zipA and ftsN can be individually deleted in ftsA* mutant cells, but the simultaneous depletion of both proteins is lethal and cells do not establish preseptal sites. Our data support a model according to which ZipA and FtsN-FtsA have semi-redundant roles in connecting the cytosolic FtsZ ring with the membrane-anchored peptidoglycan synthases during the preseptal phase of envelope growth.

摘要

在从延伸到分隔的转变过程中,大肠杆菌在未来的分裂部位建立一个环状的肽聚糖生长区。这种前间隔肽聚糖合成不需要细胞分裂特异性的肽聚糖转肽酶 PBP3 或大多数其他细胞分裂蛋白,但它确实需要 FtsZ、其膜锚定 ZipA 和至少一种双功能糖基转移酶-转肽酶,PBP1A 或 PBP1B。在这里,我们表明 PBP1A 和 PBP1B 与 ZipA 相互作用,并在 PBP3 受抑制的细胞中定位于前间隔部位。ZipA 刺激 PBP1A 的糖基转移酶活性。膜锚定的细胞分裂蛋白 FtsN 在间隔前部位定位,并刺激 PBP1B 的两种活性。可以单独删除 zipA 和 ftsN 基因在 ftsA*突变细胞中,但同时耗尽这两种蛋白质是致命的,细胞不会建立前间隔部位。我们的数据支持这样一种模型,即 ZipA 和 FtsN-FtsA 在细胞质 FtsZ 环与膜锚定肽聚糖合成酶之间的前间隔阶段连接中具有半冗余作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ca/6269477/e8ada6ec788a/41467_2018_7559_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ca/6269477/7de8975f0d47/41467_2018_7559_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ca/6269477/0a298b2a3b4b/41467_2018_7559_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ca/6269477/0b926ae24a2a/41467_2018_7559_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ca/6269477/0a352b997a05/41467_2018_7559_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ca/6269477/eac84aad0492/41467_2018_7559_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ca/6269477/e8ada6ec788a/41467_2018_7559_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ca/6269477/7de8975f0d47/41467_2018_7559_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ca/6269477/0a298b2a3b4b/41467_2018_7559_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ca/6269477/0b926ae24a2a/41467_2018_7559_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ca/6269477/0a352b997a05/41467_2018_7559_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ca/6269477/eac84aad0492/41467_2018_7559_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ca/6269477/e8ada6ec788a/41467_2018_7559_Fig6_HTML.jpg

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