Suppr超能文献

嗜热四膜虫中获得性耐热性的诱导:蛋白质合成抑制剂的作用

Induction of acquired thermotolerance in Tetrahymena thermophila: effects of protein synthesis inhibitors.

作者信息

Hallberg R L, Kraus K W, Hallberg E M

出版信息

Mol Cell Biol. 1985 Aug;5(8):2061-9. doi: 10.1128/mcb.5.8.2061-2069.1985.

Abstract

When Tetrahymena thermophila cells growing at 30 degrees C are shifted to either 40 or 43 degrees C, the kinetics and extent of induction of heat shock mRNAs in both cases are virtually indistinguishable. However, the cells shifted to 40 degrees C show a typical induction of heat shock protein (HSP) synthesis and survive indefinitely (100% after 24 h), whereas those at 43 degrees C show an abortive synthesis of HSPs and die (less than 0.01% survivors) within 1 h. Cells treated at 30 degrees C with the drugs cycloheximide or emetine, at concentrations which are initially inhibitory to protein synthesis and cell growth but from which cells can eventually recover and resume growth, are after this recovery able to survive a direct shift from 30 to 43 degrees C (ca. 70% survival after 1 h). This induction of thermotolerance by these drugs is as efficient in providing thermoprotection to cells as is a prior sublethal heat treatment which elicits the synthesis of HSPs. However, during the period when drug-treated cells recover their protein synthesis ability and simultaneously acquire the ability to subsequently survive a shift to 43 degrees C, none of the major HSPs are synthesized. The ability to survive a 1-h, 43 degrees C heat treatment, therefore, does not absolutely require the prior synthesis of HSPs. But, as extended survival at 43 degrees Celsius depends absolutely on the ability of cells to continually synthesize HSPs, it appears that a prior heat shock as well as the recovery from protein synthesis inhibition elicits a change in the protein synthetic machinery which allows the translation of HSP mRNAs at what would otherwise be a nonpermissive temperature for protein synthesis.

摘要

当在30℃生长的嗜热四膜虫细胞转移至40℃或43℃时,两种情况下热休克mRNA诱导的动力学和程度几乎无法区分。然而,转移至40℃的细胞显示出热休克蛋白(HSP)合成的典型诱导,并且能无限期存活(24小时后存活率为100%),而处于43℃的细胞则显示出HSP的异常合成,并在1小时内死亡(存活率低于0.01%)。在30℃用环己酰亚胺或依米丁处理细胞,这些药物的浓度最初会抑制蛋白质合成和细胞生长,但细胞最终能够从中恢复并恢复生长,恢复后这些细胞能够直接从30℃转移至43℃并存活(1小时后存活率约为70%)。这些药物诱导的耐热性在为细胞提供热保护方面与引发HSP合成的亚致死性热预处理一样有效。然而,在药物处理的细胞恢复其蛋白质合成能力并同时获得随后在转移至43℃后存活的能力的期间内,没有合成任何主要的HSP。因此,在43℃进行1小时热处理后存活的能力并不绝对需要预先合成HSP。但是,由于在43℃的延长存活绝对依赖于细胞持续合成HSP的能力,似乎预先的热休克以及从蛋白质合成抑制中的恢复引发了蛋白质合成机制的变化,这使得HSP mRNA能够在否则对蛋白质合成而言是非允许温度下进行翻译。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8d/366924/d0fafd0794b9/molcellb00104-0264-a.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验