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在酿酒酵母中,热耐受性与全谱热休克蛋白的诱导以及细胞周期阻滞无关。

Thermotolerance is independent of induction of the full spectrum of heat shock proteins and of cell cycle blockage in the yeast Saccharomyces cerevisiae.

作者信息

Barnes C A, Johnston G C, Singer R A

机构信息

Department of Microbiology, Dalhousie University, Halifax, Nova Scotia, Canada.

出版信息

J Bacteriol. 1990 Aug;172(8):4352-8. doi: 10.1128/jb.172.8.4352-4358.1990.

Abstract

Cells of the yeast Saccharomyces cerevisiae are known to acquire thermotolerance in response to the stresses of starvation or heat shock. We show here through the use of cell cycle inhibitors that blockage of yeast cells in the G1, S, or G2 phases of the mitotic cell cycle is not a stress that induces thermotolerance; arrested cells remained as sensitive to thermal killing as proliferating cells. These G1- or S-phase-arrested cells were unimpaired in the acquisition of thermotolerance when subjected to a mild heat shock by incubation at 37 degrees C. One cell cycle inhibitor, o-phenanthroline, did in fact cause cells to become thermotolerant but without induction of the characteristic pattern of heat shock proteins. Thermal induction of heat shock protein synthesis was unaffected; the o-phenanthroline-treated cells could still synthesize heat shock proteins upon transfer to 37 degrees C. Use of a novel mutant conditionally defective only for the resumption of proliferation from stationary phase (M. A. Drebot, G. C. Johnston, and R. A. Singer, Proc. Natl. Acad. Sci. USA 84:7948-7952, 1987) indicated that o-phenanthroline inhibition produces a stationary-phase arrest, a finding which is consistent with the increased thermotolerance and regulated cessation of proliferation exhibited by the inhibited cells. These findings show that the acquired thermotolerance of cells is unrelated to blockage of the mitotic cell cycle or to the rapid synthesis of the characteristic spectrum of heat shock proteins.

摘要

已知酿酒酵母细胞会因饥饿或热休克应激而获得耐热性。我们在此表明,通过使用细胞周期抑制剂,将酵母细胞阻滞在有丝分裂细胞周期的G1、S或G2期并非诱导耐热性的应激;停滞的细胞对热杀伤的敏感性与增殖细胞相同。当在37℃孵育进行轻度热休克时,这些G1期或S期停滞的细胞在获得耐热性方面并未受损。一种细胞周期抑制剂邻菲罗啉实际上确实使细胞变得耐热,但并未诱导热休克蛋白的特征性模式。热休克蛋白合成的热诱导不受影响;经邻菲罗啉处理的细胞在转移至37℃时仍能合成热休克蛋白。使用一种仅在从静止期恢复增殖方面有条件缺陷的新型突变体(M. A. Drebot、G. C. Johnston和R. A. Singer,《美国国家科学院院刊》84:7948 - 7952,1987)表明,邻菲罗啉抑制会导致静止期停滞,这一发现与受抑制细胞表现出的耐热性增加和增殖的调节性停止一致。这些发现表明,细胞获得的耐热性与有丝分裂细胞周期的阻滞或热休克蛋白特征谱的快速合成无关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9de7/213261/48190b018ddb/jbacter00122-0234-a.jpg

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