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通过热激和盐激诱导酿酒酵母的耐热性、抗冻性和耐盐性。

Induction of heat, freezing and salt tolerance by heat and salt shock in Saccharomyces cerevisiae.

作者信息

Lewis J G, Learmonth R P, Watson K

机构信息

Department of Biochemistry, Microbiology and Nutrition, University of New England, Armidale, Australia.

出版信息

Microbiology (Reading). 1995 Mar;141 ( Pt 3):687-94. doi: 10.1099/13500872-141-3-687.

Abstract

Stress tolerance of Saccharomyces cerevisiae was examined after exposure to heat and salt shock in the presence or absence of the protein synthesis inhibitor cycloheximide. Cells heat-shocked (37 degrees C for 45 min) in the absence of cycloheximide demonstrated increased tolerance of heat, freezing and salt stress. For cells heat-shocked in the presence of cycloheximide, heat and salt tolerance could still be induced, although at lower levels, while induction of freezing tolerance was completely inhibited. These results indicated that while heat shock proteins (hsps) may contribute to induced heat and salt tolerance they are not essential, although induction of freezing tolerance appears to require protein synthesis. Exposure of cells to salt shock (300 mM NaCl for 45 min) induced stress protein synthesis and the accumulation of glycerol, responses analogous to induction of hsp synthesis and trehalose accumulation in cells exposed to heat shock. Cells salt-shocked in the absence of cycloheximide showed a similar pattern of induced stress tolerance as with heat, with increased tolerance of heat, salt and freezing. Cells salt-shocked in the presence of cycloheximide continued to show induced heat and salt tolerance, but freezing tolerance could not be induced. These results lend support to the hypothesis that hsp synthesis is not essential for induced tolerance of some forms of stress and that accumulated solutes such as trehalose or glycerol may contribute to induced stress tolerance.

摘要

在存在或不存在蛋白质合成抑制剂环己酰亚胺的情况下,将酿酒酵母暴露于热休克和盐休克后,检测其应激耐受性。在不存在环己酰亚胺的情况下进行热休克处理(37℃,45分钟)的细胞,对热、冷冻和盐胁迫的耐受性增强。对于在环己酰亚胺存在下进行热休克处理的细胞,虽然热耐受性和盐耐受性的诱导水平较低,但仍可诱导产生,而冷冻耐受性的诱导则完全受到抑制。这些结果表明,虽然热休克蛋白(hsps)可能有助于诱导热耐受性和盐耐受性,但它们并非必不可少,尽管冷冻耐受性的诱导似乎需要蛋白质合成。将细胞暴露于盐休克(300 mM NaCl,45分钟)可诱导应激蛋白合成和甘油积累,这与暴露于热休克的细胞中hsp合成和海藻糖积累的诱导反应类似。在不存在环己酰亚胺的情况下进行盐休克处理的细胞,其诱导的应激耐受性模式与热休克处理相似,对热、盐和冷冻的耐受性均增强。在环己酰亚胺存在下进行盐休克处理的细胞,继续表现出诱导的热耐受性和盐耐受性,但无法诱导出冷冻耐受性。这些结果支持了以下假设:hsp合成对于某些形式的应激诱导耐受性并非必不可少,并且积累的溶质(如海藻糖或甘油)可能有助于诱导应激耐受性。

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