Transcriptional and translational regulation of major heat shock proteins and patterns of trehalose mobilization during hyperthermic recovery in repressed and derepressed Saccharomyces cerevisiae
Transcriptional and translational regulation of major heat shock proteins and patterns of trehalose mobilization during hyperthermic recovery in repressed and derepressed Saccharomyces cerevisiae
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DOI：
10.1139/cjm-44-4-341
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发表时间：
1998-04-01
影响因子：
2.8
通讯作者：
Watson, K
中科院分区：
文献类型：
--
作者：
Gross, C;Watson, K
在热休克期间以及随后将细胞返回到 25°C 期间，研究了酿酒酵母的葡萄糖（抑制）和醋酸盐（去抑制）生长细胞中的热休克基因转录和翻译模式以及海藻糖含量。热休克细胞（37°C，30 分钟）在补充葡萄糖或醋酸盐的培养基中生长，最初获得了对 50°C 热应激的高耐热性，这种耐热性逐渐增强。当培养物在 25 摄氏度下恢复并随后暴露于第二次热应激时，就会丢失。在所有情况下，除了相对热敏感菌株的抑制细胞外，热休克过程中蛋白质合成的抑制和海藻糖积累的同时减少对耐热性丧失的动力学影响很小。 37 摄氏度的听觉休克会导致编码主要热休克蛋白 (hsps) 的基因的转录和翻译显着增加。在 25°C 恢复期间，两种代谢活动均受到抑制，随后 hsp mRNA 转录逐渐增加至热激前观察到的水平。然而，尽管免疫检测分析表明在整个 240 分钟恢复期内细胞中持续存在高水平的 hsp 104、90、70 和 60，但在恢复阶段不再观察到 hsp mRNA 的从头翻译。此外，虽然热休克诱导的海藻糖在抑制细胞的恢复过程中迅速降解，但在去抑制细胞中水平仍然很高。因此，结果表明，葡萄糖和乙酸盐生长的细胞所表现出的诱导耐热性的逐渐丧失与hsp或海藻糖的水平并不密切相关。结论是，组成型和从头合成的热休克蛋白都需要热休克相关的激活来赋予耐热性，并且这种修饰在从热休克状态释放后逐渐逆转。
Patterns of heat shock gene transcription and translation, as well as trehalose content, were investigated in both glucose (repressed) and acetate (derepressed) grown cells of Saccharomyces cerevisiae during heat shock and subsequent return of cells to 25 degrees C. Heat-shocked cells (37 degrees C for 30 min), grown in either glucose- or acetate-supplemented media, initially acquired high thermotolerance to a 50 degrees C heat stress, which was progressively lost when cultures were allowed to recover at 25 degrees C and subsequently exposed to a second heat stress. In all cases, with the notable exception of repressed cells of a relatively thermosensitive strain, inhibition of protein synthesis and coincident decrease in trehalose accumulation during the heat shock had little effect on the kinetics of loss of thermotolerance. Hear shock at 37 degrees C elicited a marked increase in transcription and translation of genes encoding major heat shock proteins (hsps). During recovery at 25 degrees C, both metabolic activities were suppressed followed by a gradual increase in hsp mRNA transcription to levels observed prior to heat shock. De novo translation of hsp mRNAs, however, was no longer observed during the recovery phase, although immunodetection analyses demonstrated persistence of high levels of hsps 104, 90, 70, and 60 in cells throughout the 240-min recovery period. In addition, while heat shock induced trehalose was rapidly degraded during recovery in repressed cells, levels remained high in derepressed cells. Results therefore indicated that the progressive loss of induced thermotolerance exhibited by glucose- and acetate-grown cells was not closely correlated with levels of hsp or trehalose. It was concluded that both constitutive and de novo synthesized hsps require heat shock associated activation to confer thermotolerance and this modification is progressively reversed upon release from the heat-shocked state.