The ability to recover components of their own cell wall is a common feature of bacteria. This was initially recognized in the Gram-negative bacterium Escherichia coli, which recycles about half of the peptidoglycan of its cell wall during one cell doubling. Moreover, E. coli was shown to grow on peptidoglycan components provided as nutrients. A distinguished recycling enzyme of E. coli required for both, recovery of the cell wall sugar N-acetylmuramic acid (MurNAc) of the own cell wall and for growth on external MurNAc, is the MurNAc 6-phosphate (MurNAc 6P) lactyl ether hydrolase MurQ. We revealed however, that most Gram-negative bacteria lack a murQ ortholog and instead harbor a pathway, absent in E. coli, that channels MurNAc directly to peptidoglycan biosynthesis. This “anabolic recycling pathway" bypasses the initial steps of peptidoglycan de novo synthesis, including the target of the antibiotic fosfomycin, thus providing intrinsic resistance to the antibiotic. The Gram-negative oral pathogen Tannerella forsythia is auxotrophic for MurNAc and apparently depends on the anabolic recycling pathway to synthesize its own cell wall by scavenging cell wall debris of other bacteria. In contrast, Gram-positive bacteria lack the anabolic recycling genes, but mostly contain one or two murQ orthologs. Quantification of MurNAc 6P accumulation in murQ mutant cells by mass spectrometry allowed us to demonstrate for the first time that Gram-positive bacteria do recycle their own peptidoglycan. This had been questioned earlier, since peptidoglycan turnover products accumulate in the spent media of Gram-positives. We showed, that these fragments are recovered during nutrient limitation, which prolongs starvation survival of Bacillus subtilis and Staphylococcus aureus. Peptidoglycan recycling in these bacteria however differs, as the cell wall is either cleaved exhaustively and monosaccharide building blocks are taken up (B. subtilis) or disaccharides are released and recycled involving a novel phosphomuramidase (MupG; S.aureus). In B. subtilis also the teichoic acids, covalently bound to the peptidoglycan (wall teichoic acids; WTAs), are recycled. During phosphate limitation, the sn-glycerol-3-phosphate phosphodiesterase GlpQ specifically degrades WTAs of B. subtilis. In S. aureus, in contrast, GlpQ is used to scavenge external teichoic acid sources. Thus, although bacteria generally recover their own cell wall, they apparently apply distinct strategies for breakdown and reutilization of cell wall fragments. This review summarizes our work on this topic funded between 2011 and 2019 by the DFG within the collaborative research center SFB766.

恢复自身细胞壁成分的能力是细菌的普遍特征。最初在革兰氏阴性细菌大肠埃希氏菌中得到识别，该细菌在一个细胞加倍过程中回收了其细胞壁约一半的肽聚糖。此外，显示大肠杆菌在作为营养素提供的肽聚糖成分上生长。回收自身细胞壁的细胞壁糖N-乙酰基尿酸（MurNAc）以及在外部MurNAc上生长所需的一种独特的大肠杆菌再循环酶是MurNAc 6-磷酸酯（MurNAc 6P）乳酸醚水解酶。 MurQ。但是，我们发现，大多数革兰氏阴性细菌缺乏murQ直系同源基因，而是具有一条通路，不存在在大肠杆菌中，它将MurNAc直接引导至肽聚糖的生物合成。这种“合成代谢再循环途径”绕过的肽聚糖的初始步骤从头合成，包括抗生素磷霉素的目标，从而对抗生素提供固有电阻。革兰氏阴性口腔病原体福赛斯坦纳菌是营养缺陷的MurNAc和显然依赖于合成代谢革兰氏阳性细菌缺乏合成代谢的再循环基因，但主要含有一或两个murQ直系同源物，对murQ中MurNAc 6P积累的定量分析质谱分析突变细胞使我们首次证明革兰氏阳性细菌确实回收了其自身的肽聚糖。由于肽聚糖周转产物积聚在革兰氏阳性的废培养基中，这早已受到质疑。我们表明，这些片段在营养限制期间得以恢复，从而延长了枯草芽孢杆菌和金黄色葡萄球菌的饥饿生存时间。肽聚糖回收在这些细菌然而不同，因为细胞壁要么详尽裂解和单糖积木被吸收（枯草芽孢杆菌）或二糖被释放和回收涉及新颖phosphomuramidase（MupG;金黄色葡萄球菌）。在枯草芽孢杆菌中还回收了与肽聚糖共价键合的邻苯二酸（壁邻苯二甲酸； WTA）。在磷酸盐限制期间，sn-甘油-3-磷酸磷酸二酯酶GlpQ特异性降解枯草芽孢杆菌的WTA 。相比之下，在金黄色葡萄球菌中，GlpQ用于清除外来的chochoicic酸源。因此，尽管细菌通常恢复其自身的细胞壁，但显然它们对细胞壁片段的分解和再利用采取了不同的策略。这篇综述总结了我们在合作研究中心SFB766内由DFG资助的2011年至2019年有关该主题的工作。