Toxin-antitoxin (TA) systems are ubiquitous genetic elements in bacterial genomes, but their functions are controversial. Although they are frequently postulated to regulate cell growth following stress, few null phenotypes for TA systems have been reported. Here, we show that TA transcript levels can increase substantially in response to stress, but toxin is not liberated. We find that the growth of an Escherichia coli strain lacking ten TA systems encoding endoribonuclease toxins is not affected following exposure to six stresses that each trigger TA transcription. Additionally, using RNA sequencing, we find no evidence of mRNA cleavage following stress. Stress-induced transcription arises from antitoxin degradation and relief of transcriptional autoregulation. Importantly, although free antitoxin is readily degraded in vivo, antitoxin bound to toxin is protected from proteolysis, preventing release of active toxin. Thus, transcription is not a reliable marker of TA activity, and TA systems do not strongly promote survival following individual stresses.

毒素-抗毒素（TA）系统是细菌基因组中普遍存在的遗传元件，但其功能存在争议。尽管经常假设它们在应激后调节细胞生长，但很少有 TA 系统无效表型的报道。在这里，我们发现 TA 转录水平可以因应对压力而大幅增加，但毒素不会释放。我们发现，缺乏十个编码内切核糖核酸酶毒素的 TA 系统的大肠杆菌菌株在暴露于六种应激（每种应激均触发 TA 转录）后，其生长不会受到影响。此外，通过 RNA 测序，我们没有发现压力后 mRNA 裂解的证据。应激诱导的转录源于抗毒素降解和转录自动调节的缓解。重要的是，尽管游离抗毒素在体内很容易降解，但与毒素结合的抗毒素受到保护免于蛋白水解，从而防止活性毒素的释放。因此，转录并不是 TA 活性的可靠标记，并且 TA 系统不会强烈促进个体应激后的生存。