The nine toxin families.

The targets and the types of activities of the nine toxins as well as the cellular processes that are affected by the expression of the toxins are shown. This table is adapted from [7] except where indicated. ND, not determined.
1The CcdB toxin does not generate double-strand breaks by itself. Overexpression of CcdB inhibits the re-ligation step of the DNA gyrase, a type II topoisomerase, which leads to the generation of double-strand breaks.
2Overexpression of RelE induces cleavage of mRNAs at the ribosome A-site.
3,4ParE was shown to poison DNA gyrase and to generate double-strand breaks in vitro.
5As CcdB, it induces inhibition of cell division and therefore, it is assumed that it inhibits replication.
6Overproduction of the Doc toxin activates the relBE TA system and indirectly causes mRNA cleavage [53].
7Doc inhibits translation elongation by association with the 30S ribosomal subunit [54].
8See [55]. Although VapC shows an endoribonucleolytic activity, it has not been reported whether or not VapC is able to inhibit translation.
9The ζ toxin is part of a three-component TA system (ω−ε−ζ) in which the antitoxin and autoregulation properties are encoded by separate polypeptides.
10See [56].
11At a high overexpression level, the ζ toxin inhibits replication, transcription, and translation, eventually leading to cell death [57]. However, the specific target(s) is (are) unknown.
12See [34].
13See [33].
14See [32],[33],[34].
15The genetic organisation of the higBA system is unusual; the toxin gene is upstream of the antitoxin gene in the operon.
16,17See [40],[58].

本表格展示了9种毒素的作用靶点、活性类型，以及毒素表达所影响的细胞生物学过程。本表格改编自文献[7]，除另有标注外。ND即未测定（not determined）。
1. CcdB毒素本身无法产生双链断裂。过表达CcdB会抑制II型拓扑异构酶DNA旋转酶的再连接步骤，进而引发双链断裂的产生。
2. RelE过表达可诱导核糖体A位点处的mRNA裂解。
3、4. 已有研究证实ParE可抑制DNA旋转酶活性，并在体外诱导双链断裂生成。
5. 与CcdB类似，该毒素可抑制细胞分裂，因此推测其可阻断DNA复制过程。
6. Doc毒素的过量表达会激活relBE毒素-抗毒素（toxin-antitoxin，TA）系统，并间接引发mRNA裂解[53]。
7. Doc可通过与30S核糖体亚基结合，抑制翻译延伸过程[54]。
8. 详见文献[55]。尽管VapC具有核糖核酸内切酶活性，但目前尚无研究报道VapC具备抑制翻译的能力。
9. ζ毒素属于三组分TA系统（ω−ε−ζ）的组成部分，该系统的抗毒素与自主调控功能由独立的多肽编码。
10. 详见文献[56]。
11. 在高过表达水平下，ζ毒素可抑制DNA复制、转录与翻译过程，最终导致细胞死亡[57]，但其具体作用靶点尚未明确。
12. 详见文献[34]。
13. 详见文献[33]。
14. 详见文献[32]、[33]、[34]。
15. higBA系统的基因排布较为特殊：毒素基因位于操纵子内抗毒素基因的上游。
16、17. 详见文献[40]、[58]。