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首页> 外文期刊>Journal of bacteriology >Killer toxin for sake yeast: properties and effects of adenosine 5'-diphosphate and calcium ion on killing action.
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Killer toxin for sake yeast: properties and effects of adenosine 5'-diphosphate and calcium ion on killing action.

机译:杀手毒素的粘液酵母:腺苷5'-二磷酸盐和钙离子对杀灭作用的性质和影响。

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The killer character of strain isolated from the main mash of sake brewing which produces a killer substance for sake yeast was transmitted to hybrids of the strain and a standard strain of Saccharomyces cerevisiae through a cytoplasmic determinant. The character was eliminated at 41 degrees C by incubation followed by growth at 30 degrees C. The killer strain produced the killer toxin in a growth-associated manner. A preparation of crude killer toxin extract showed first-order inactivation and a linear Arrhenius plot between 25 and 40 degrees C, with an activation of energy of 55.0 kcal/mol. Addition of 1% of synthetic polymer protected the toxin from inactivation by agitation but not by heat. Enhancement of the killer action toward sensitive yeast cells by only the nucleotide adenosine 5'-diphosphate (ADP) was observed after plating on agar medium as well as after incubation in liquid medium. The addition of CaCl2 reversed the enhancing effect of ADP on killing activity. This action of CaCl2 was inhibited by cycloheximide, suggesting that protein synthesis is required for recovery of toxin-induced cells in the presence of CaCl2. Further, CaCl2 overcame the decrease in the intracellular level of adenosine 5'-triphosphate (ATP) enhanced by ADP in killer-treated cells and also inhibited leakage of ATP from the cells with immediate response. The mode of killing action is discussed in terms of a transient state of the cells and the action of ADP and CaCl2.
机译:从Sake酿造的主要醪中分离的菌株的杀伤特征,通过细胞质决定簇传递给粘液酵母的杀伤物质和菌株的杂交物和酿酒酵母的标准菌株。通过孵育在41℃下除去特征,然后在30摄氏度下生长。杀伤菌株以生长相关的方式产生杀伤毒素。粗杀毒素毒素提取物的制备显示了一阶失活和25至40℃之间的线性arrhenius图,其能量为55.0kcal / mol。添加1%的合成聚合物保护毒素通过搅拌而不是通过热量灭活。在琼脂培养基上仅观察到在琼脂培养基上观察核苷酸腺苷12'-二磷酸(ADP)对敏感酵母细胞的增强以及在液体培养基中孵育后观察到敏感酵母细胞。加入CaCl2逆转了ADP对杀害活动的增强作用。 CaCl2的该作用由环己酰亚胺抑制,表明在CaCl 2存在下需要蛋白质合成来恢复毒素诱导的细胞。此外,CaCl2克服通过杀手处理细胞中的ADP增强的腺苷5'-三磷酸(ATP)的细胞内水平的降低,并且还抑制了响应的响应从细胞中的ATP泄漏。就细胞的瞬态状态和ADP和CACL2的作用而言,讨论了杀灭作用的模式。

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