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Lack of correlation between trehalose accumulation, cell viability and intracellular acidification as induced by various stresses in Saccharomyces cerevisiae

机译:在酵母菌酿酒酵母中诱导的海藻糖积累,细胞活力和细胞内酸之间的相关性缺乏相关性

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A pma1-1 mutant of Saccharomyces cerevisiae with reduced H+-ATPase activity and the isogenic wild-type strain accumulated high levels of trehalose in response to a temperature upshift to 40 éC and after addition of 10% ethanol, but only modest levels in response to a rapid drop in external pH and after addition of decanoic acid. There was, however, no correlation between the absolute levels of trehalose in the stressed cells and their viability. All these treatments induced a significant decrease in intracellular pH, and surprisingly, this decrease was very similar in both strains, indicating that intracellular acidification could not be the triggering mechanism for trehalose accumulation in response to stress. A careful investigation of metabolic parameters was carried out to explain how trehalose accumulated under the four different stress conditions tested. No single and common mechanism for trehalose accumulation could be put forward and the transcriptional activation of TPS1 was not unequivocally related to trehalose accumulation. Another finding was that a pma1-1 mutant exhibited a two- to threefold greater capacity to accumulate trehalose than the isogenic wild-type. This enhanced disaccharide synthesis could be attributed to a twofold higher trehalose-6-phosphate synthase activity, together with a fourfold higher content of intracellular UDP-Glc. In addition, this mutant showed 1.5-fold higher levels of ATP compared to the wild-type. The various stress treatments studied showed that a drop in intracellular pH does not correlate with trehalose accumulation. It is suggested that plasma membrane alteration could be the physiological trigger inducing trehalose accumulation in yeast.
机译:具有降低的H + -ATPase活性的酿酒酵母的PMA1-1突变体,并响应于40éc和加入10%乙醇后,响应于40éc,但响应于外部pH的快速下降和加入癸酸后。然而,在应激细胞中的海藻糖的绝对水平与其活力之间没有相关性。所有这些治疗诱导细胞内pH的显着降低,令人惊讶的是,这种降低在两个菌株中非常相似,表明细胞内酸化不能是对胁迫响应胁迫的海藻糖积累的触发机制。进行了对代谢参数的仔细研究,以解释在测试的四种不同应力条件下积累的海藻糖。不能提出单一和常见的海藻糖积累机制,TPS1的转录激活与海藻糖积累并不明确相关。另一种发现是PMA1-1突变体表现出两到三倍的容量,以积累海藻糖而不是中源性野生型。这种增强的二糖合成可归因于双重海藻糖-6-磷酸合酶活性,以及​​细胞内UDP-GLC的四倍较高含量。此外,与野生型相比,该突变体显示出1.5倍较高的ATP水平。研究的各种应力处理表明,细胞内pH下降与海藻糖积累不相关。建议血浆膜改变可以是诱导酵母中海藻累积的生理触发。

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