Gotfredsen M, Gerdes K
Department of Molecular Biology, Odense University, Odense M, Denmark.
Mol Microbiol. 1998 Aug;29(4):1065-76. doi: 10.1046/j.1365-2958.1998.00993.x.
Toxin-antitoxin systems are defined as a group of plasmid- and chromosome-encoded loci that specify a cell toxin and a protein antitoxin. Plasmid-encoded toxin-antitoxin systems stabilize their replicons by killing plasmid-free cells. Here, we show that the relBE genes of Escherichia coli K-12 have all the basic features previously connected with toxin-antitoxin systems: (i) relE encodes a cytotoxin lethal or inhibitory to host cells; (ii) relB encodes an antitoxin that prevents the lethal action of the relE-encoded toxin; (iii) the relBE genes stabilize a mini-R1 test plasmid; and (iv) the RelB antitoxin autoregulates the relBEF operon at the level of transcription. Using database searching, we found relBE homologues on the chromosomes of E. coli K-12, Haemophilus influenzae and Vibrio cholerae. A fifth relBE homologue was identified on the enterotoxin encoding E. coli plasmid P307. Indirect evidence suggests that the toxicity of RelE may be related to the inhibition of protein synthesis. Based on these observations, we propose a model that explains the delayed relaxed phenotype associated with mutations in relB.
毒素-抗毒素系统被定义为一组由质粒和染色体编码的位点，这些位点可产生一种细胞毒素和一种蛋白质抗毒素。质粒编码的毒素-抗毒素系统通过杀死不含质粒的细胞来稳定其复制子。在此，我们表明大肠杆菌K-12的relBE基因具有先前与毒素-抗毒素系统相关的所有基本特征：（i）relE编码对宿主细胞具有致死性或抑制性的细胞毒素；（ii）relB编码一种抗毒素，可阻止relE编码毒素的致死作用；（iii）relBE基因可稳定一个mini-R1测试质粒；（iv）RelB抗毒素在转录水平上对relBEF操纵子进行自我调节。通过数据库搜索，我们在大肠杆菌K-12、流感嗜血杆菌和霍乱弧菌的染色体上发现了relBE同源物。在编码大肠杆菌肠毒素的质粒P307上鉴定出了第五个relBE同源物。间接证据表明RelE的毒性可能与蛋白质合成的抑制有关。基于这些观察结果，我们提出了一个模型，该模型解释了与relB突变相关的延迟松弛表型。
