翻译过程中核糖体停滞显著降低细胞活力,因为细胞必须花费资源合成新的核糖体。因此,所有细菌都发展了各种核糖体拯救机制。通常,核糖体的释放之前是tRNA-肽键的水解,但是,在某些情况下,由于某些因素的活性,核糖体可以继续翻译。这篇综述描述了核糖体拯救的机制,这要归功于转译和ArfA的活性,ArfB,Brfa,ArfT,HflX,和RqcP/H因子,以及通过EF-P的作用继续翻译,EF-4和EttA。尽管某些系统能够相互复制,它们中的大多数都有其独特的功能作用,有关的质量控制细菌翻译的某些异常引起的突变,胁迫栽培条件,或者抗生素.
Ribosome stalling during translation significantly reduces cell viability, because cells have to spend resources on the synthesis of new ribosomes. Therefore, all bacteria have developed various mechanisms of ribosome rescue. Usually, the release of ribosomes is preceded by hydrolysis of the tRNA-peptide bond, but, in some cases, the ribosome can continue translation thanks to the activity of certain factors. This review describes the mechanisms of ribosome rescue thanks to trans-translation and the activity of the ArfA, ArfB, BrfA, ArfT, HflX, and RqcP/H factors, as well as continuation of translation via the action of EF-P, EF-4, and EttA. Despite the ability of some systems to duplicate each other, most of them have their unique functional role, related to the quality control of bacterial translation in certain abnormalities caused by mutations, stress cultivation conditions, or antibiotics.