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Alterations in cellular lipids may be responsible for the transient nature of the yeast heat shock response

机译:细胞脂质的改变可能对酵母热休克反应的瞬态性质负责

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Summary: The stress-sensing systems leading to the cellular heat shock response (HSR) and the mechanism responsible for the desensitizing of this response in stress-acclimated cells are largely unknown. Here it is demonstrated that there is a close correlation between a 3 ° increase in the temperature required for maximal activation of a heat-shock (HS)-inducible gene in Saccharomyces cerevisiae and an increase in the percentage of cellular unsaturated fatty acids when cells are subjected to extended periods of growth at 37 °. The latter occurs with the same kinetics as HS gene down-regulation during a prolonged HS and is reversed by reacclimation to growth at 25 °. The transient nature of the HS may therefore be due to a lipid-mediated decrease in cellular heat sensitivity. Further evidence that unsaturated fatty acids desensitize cells to heat, with a resultant down-regulation of the HSR, is provided by demonstrating a 9 ° increase in the temperature required for maximal induction of this HS-inducible gene in cells containing high levels of unsaturated fatty acids assimilated during anaerobic growth at 25 °.
机译:发明内容:导致细胞热休克响应(HSR)的应力感测系统和负责在应力 - 适应的细胞中对该响应的脱敏的机制在很大程度上是未知的。在这里证明,在糖酵母酿酒酵母中最大激活热冲击(HS)-uducibe基因的最大激活所需的温度之间存在紧密相关性,并且当细胞是细胞不饱和脂肪酸的百分比增加在37°延长延长的生长期。后者发生在延长的HS期间的HS基因下调相同的动力学,并通过重新加入在25°处的生长逆转。因此,HS的瞬态性质可能是由于细胞热敏感性的脂质介导的降低。进一步的证据表明,不饱和脂肪酸将细胞与HSR的所得下调进行了加热,通过说明在含有高水平不饱和脂肪含量的细胞中最大诱导的温度的温度增加9°酸在25°处的厌氧生长期间同化化。

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