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低温对酿酒酵母磷脂突变体活力的影响。

Effect of low temperature upon vitality of Saccharomyces cerevisiae phospholipid mutants.

机构信息

Biotecnologia Enológica, Departament de Bioquimica i Biotecnologia, Facultat de Enologia, Universitat Rovira i Virgili, Tarragona, Spain.

出版信息

Yeast. 2012 Oct;29(10):443-52. doi: 10.1002/yea.2924. Epub 2012 Oct 1.

Abstract

The phospholipid metabolism of Saccharomyces cerevisiae plays a central role in its adaptation to low temperatures. In order to detect the key genes in this adaptation, various phospholipid mutants from the EUROSCARF collection of Saccharomyces cerevisiae BY4742 were tested to ascertain whether the suppression of some genes could improve the fermentation vitality of the cells at low temperature. The cell vitality and phospholipid composition of these mutants were analysed. Some knockouts improved (hmn1Δ) or impaired (cho2Δ and psd1Δ) their vitality at low temperature (13 ° C) but were not affected at optimum temperature (25 ° C). A common trait of the mutants that had some defect in vitality was a lower concentration of phosphatidylcholine and/or phosphatidylethanolamine. The supplementation with choline allowed them to recover viability, probably by synthesis through the Kennedy pathway. Hmn1Δ showed a lower concentration of phosphatidylcholine, which explains the dominant role of the de novo pathway in cellular phosphatidylethanolamine and phosphatidylcholine vs the Kennedy pathway. The absence of such genes as CRD1 or OPI3 produced important changes in phospholipid composition. Cardiolipin was not detected in crd1Δ but phosphatidylglycerol circumvents most of the functions assigned to CL. The considerable reduction in PC diminished the cell vitality of opi3Δ at both temperatures, although the decrease at 13 ° C was more marked.

摘要

酿酒酵母的磷脂代谢在其适应低温中起着核心作用。为了检测这种适应过程中的关键基因,对 EUROSCARF 酿酒酵母 BY4742 磷脂突变体库中的各种突变体进行了测试,以确定抑制某些基因是否可以提高细胞在低温下的发酵活力。分析了这些突变体的细胞活力和磷脂组成。一些敲除突变体提高了(hmn1Δ)或损害了(cho2Δ 和 psd1Δ)细胞在低温(13°C)下的活力,但在最佳温度(25°C)下不受影响。活力存在某些缺陷的突变体的一个共同特征是磷脂酰胆碱和/或磷脂酰乙醇胺的浓度较低。用胆碱补充可以恢复它们的活力,可能是通过 Kennedy 途径合成的。Hmn1Δ 表现出较低的磷脂酰胆碱浓度,这解释了从头途径在细胞磷脂酰乙醇胺和磷脂酰胆碱与 Kennedy 途径中的主导作用。缺乏 CRD1 或 OPI3 等基因会导致磷脂组成发生重要变化。crd1Δ 中未检测到心磷脂,但磷脂酰甘油可规避 CL 分配的大部分功能。在两种温度下,opi3Δ 中 PC 的大量减少降低了细胞活力,尽管在 13°C 时下降更为明显。

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