Friedrich-Schiller-Universität Jena, Lehrstuhl für Genetik, AG Bakteriengenetik, Philosophenweg 12, D-07743 Jena, Germany.
Toxins (Basel). 2018 Feb 7;10(2):74. doi: 10.3390/toxins10020074.
/SR6 is the second type I toxin-antitoxin (TA) system encoded on prophage SPβ in the chromosome. The ORF specifying a 58 aa toxin is transcribed on a polycistronic mRNA under control of the promoter. The antitoxin SR6 is a 100 nt antisense RNA that overlaps at its 3' end and the downstream gene encoding a second, much weaker, toxin at its 5' end. SR6 displays a half-life of >60 min, whereas mRNA is less stable with a half-life of ≈8 min. SR6 is in significant excess over mRNA except in minimal medium with glucose. It interacts with the 3' UTR of mRNA, thereby promoting its degradation by RNase III. By contrast, SR6 does not affect the amount or half-life of mRNA. However, in its absence, a overexpression plasmid could not be established in suggesting that SR6 inhibits translation by directly binding to its ribosome-binding site. While the amounts of both RNA and SR6 were affected by vancomycin, manganese, heat-shock and ethanol stress as well as iron limitation, oxygen stress decreased only the amount of SR6.
/SR6 是染色体上噬菌体 SPβ 编码的第二型 I 类毒素-抗毒素（TA）系统。指定一个 58 个氨基酸毒素的 ORF 在启动子的控制下转录于多顺反子 mRNA 上。抗毒素 SR6 是一个 100nt 的反义 RNA，其 3'端与下游基因重叠，下游基因编码第二个较弱的毒素。SR6 的半衰期>60 分钟，而 mRNA 不太稳定，半衰期约为 8 分钟。除了在葡萄糖的基础培养基中，SR6 的含量大大超过 mRNA。它与 mRNA 的 3'UTR 相互作用，从而促进其被 RNase III 降解。相比之下，SR6 不会影响 mRNA 的数量或半衰期。然而，在其缺失的情况下，无法在 中建立 的过表达质粒，这表明 SR6 通过直接结合其核糖体结合位点来抑制 的翻译。尽管万古霉素、锰、热休克和乙醇应激以及铁限制都会影响 RNA 和 SR6 的含量，但只有氧应激会降低 SR6 的含量。
