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L-丝氨酸脱氨酶缺乏会干扰大肠杆菌 K-12 的一碳代谢和细胞壁合成。

Deficiency in L-serine deaminase interferes with one-carbon metabolism and cell wall synthesis in Escherichia coli K-12.

机构信息

Biology Department, Concordia University, 1455 de Maisonneuve Ave., Montreal, Quebec H3G 1M8, Canada.

出版信息

J Bacteriol. 2010 Oct;192(20):5515-25. doi: 10.1128/JB.00748-10. Epub 2010 Aug 20.

DOI:10.1128/JB.00748-10
PMID:20729359
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2950509/
Abstract

Escherichia coli K-12 provided with glucose and a mixture of amino acids depletes L-serine more quickly than any other amino acid even in the presence of ammonium sulfate. A mutant without three 4Fe4S L-serine deaminases (SdaA, SdaB, and TdcG) of E. coli K-12 is unable to do this. The high level of L-serine that accumulates when such a mutant is exposed to amino acid mixtures starves the cells for C(1) units and interferes with cell wall synthesis. We suggest that at high concentrations, L-serine decreases synthesis of UDP-N-acetylmuramate-L-alanine by the murC-encoded ligase, weakening the cell wall and producing misshapen cells and lysis. The inhibition by high L-serine is overcome in several ways: by a large concentration of L-alanine, by overproducing MurC together with a low concentration of L-alanine, and by overproducing FtsW, thus promoting septal assembly and also by overexpression of the glycine cleavage operon. S-Adenosylmethionine reduces lysis and allows an extensive increase in biomass without improving cell division. This suggests that E. coli has a metabolic trigger for cell division. Without that reaction, if no other inhibition occurs, other metabolic functions can continue and cells can elongate and replicate their DNA, reaching at least 180 times their usual length, but cannot divide.

摘要

大肠杆菌 K-12 在提供葡萄糖和混合氨基酸的情况下,即使存在硫酸铵,也比任何其他氨基酸更快地耗尽 L-丝氨酸。大肠杆菌 K-12 中没有三种 4Fe4S L-丝氨酸脱氨酶(SdaA、SdaB 和 TdcG)的突变体无法做到这一点。当这样的突变体暴露在氨基酸混合物中时,会积累大量的 L-丝氨酸,使细胞饥饿 C(1) 单位并干扰细胞壁合成。我们认为,在高浓度下,L-丝氨酸会降低由 murC 编码的连接酶合成 UDP-N-乙酰胞壁酸-L-丙氨酸,从而削弱细胞壁并产生畸形细胞和裂解。通过几种方式克服高浓度 L-丝氨酸的抑制作用:通过大量的 L-丙氨酸、与低浓度 L-丙氨酸一起过量产生 MurC 以及过量产生 FtsW,从而促进隔膜组装,还可以通过糖裂解操纵子的过度表达。S-腺苷甲硫氨酸可减少裂解并允许大量增加生物量,而不会改善细胞分裂。这表明大肠杆菌有一种用于细胞分裂的代谢触发因素。如果没有该反应,在没有其他抑制发生的情况下,其他代谢功能可以继续进行,细胞可以伸长并复制其 DNA,达到至少 180 倍的通常长度,但不能分裂。

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本文引用的文献

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Deficiency in l-serine deaminase results in abnormal growth and cell division of Escherichia coli K-12.L-丝氨酸脱氨酶缺乏会导致大肠杆菌K-12生长异常和细胞分裂异常。
Mol Microbiol. 2008 Aug;69(4):870-81. doi: 10.1111/j.1365-2958.2008.06315.x. Epub 2008 Jun 4.
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Bacterial peptidoglycan (murein) hydrolases.细菌肽聚糖(胞壁质)水解酶
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Cytoplasmic steps of peptidoglycan biosynthesis.肽聚糖生物合成的胞质步骤。
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Peptidoglycan structure and architecture.肽聚糖的结构与架构。
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The monofunctional glycosyltransferase of Escherichia coli localizes to the cell division site and interacts with penicillin-binding protein 3, FtsW, and FtsN.大肠杆菌的单功能糖基转移酶定位于细胞分裂位点,并与青霉素结合蛋白3、FtsW和FtsN相互作用。
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Mutants, suppressors, and wrinkled colonies: mutant alleles of the cell division gene ftsQ point to functional domains in FtsQ and a role for domain 1C of FtsA in divisome assembly.突变体、抑制子与皱缩菌落:细胞分裂基因ftsQ的突变等位基因指向FtsQ中的功能结构域以及FtsA的1C结构域在分裂体组装中的作用。
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Complete set of ORF clones of Escherichia coli ASKA library (a complete set of E. coli K-12 ORF archive): unique resources for biological research.大肠杆菌ASKA文库的全套开放阅读框克隆(大肠杆菌K-12开放阅读框文库全集):生物学研究的独特资源。
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