首页> 美国卫生研究院文献>Journal of Bacteriology >Effect of cerulenin on cellular autolytic activity and lipid metabolism during inhibition of protein synthesis in Streptococcus faecalis.
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Effect of cerulenin on cellular autolytic activity and lipid metabolism during inhibition of protein synthesis in Streptococcus faecalis.

机译:铜蓝蛋白对粪便链球菌蛋白质合成抑制过程中细胞自溶活性和脂质代谢的影响。

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摘要

Cellular autolytic activity as well as lipid and lipoteichoic acid metabolism have been studied in cultures of Streptococcus faecalis receiving various combinations of the following treatments: chloramphenicol addition, starvation for an essential amino acid (valine), and cerulenin treatment. Lipoteichoic acid initially accumulated in chloramphenicol-treated and amino acid-starved cells and decreased relative to the cellular mass in cerulenin-treated cells. The relative phosphatidylglycerol content of amino acid-starved cultures or of cultures treated with either antibiotic rapidly decreased upon initiation of each treatment. In all cases, cerulenin initially stimulated diphosphatidylglycerol synthesis. Pretreatment of cultures with cerulenin prevented the inhibition of cellular synthesis autolysis normally observed during chloramphenicol treatment, but did not affect amino acid starvation-induced inhibition of autolytic activity. Variations in the levels of the nonionic lipid fraction, predominantly diglycerides, correlated best with the patterns of autolytic activity observed during chloramphenicol treatment, whereas variations in the levels of diphosphatidylglycerol and lipoteichoic acid correlated best with the patterns of autolytic activity observed during amino acid starvation. Components of the nonionic lipid fraction were demonstrated to inhibit autolytic activity 50% in whole cell and in cell wall assays at 60 and 120 nmol/mg (dry weight), respectively.
机译:已经在粪便链球菌的培养物中研究了细胞自溶活性以及脂质和脂蛋白酸的代谢,这些培养物接受以下处理的各种组合:添加氯霉素,饥饿以获取必需氨基酸(缬氨酸)和青霉素。脂磷壁酸最初在氯霉素处理和缺乏氨基酸的细胞中积累,相对于在蓝精素处理的细胞中的细胞量而言降低。在每次处理开始后,氨基酸匮乏的培养物或用任一种抗生素处理的培养物的相对磷脂酰甘油含量迅速降低。在所有情况下,铜蓝蛋白最初都会刺激二磷脂酰甘油的合成。铜蓝蛋白对培养物的预处理可防止通常在氯霉素处理过程中观察到的细胞合成自溶的抑制,但不会影响氨基酸饥饿诱导的自溶活性的抑制。非离子脂质组分的水平变化(主要是甘油二酯)与氯霉素处理过程中观察到的自溶活性模式最相关,而二磷脂酰甘油和脂蛋白酸水平的变化与氨基酸饥饿期间观察到的自溶活性模式最相关。非离子脂质组分的成分在全细胞和细胞壁测定中分别以60和120 nmol / mg(干重)抑制50%的自溶活性。

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