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莱氏无胆甾原体B中的大分子合成与胸腺嘧啶饥饿死亡

Macromolecular synthesis and thymineless death in Mycoplasma laidlawii B.

作者信息

Smith D W, Hanawalt P C

出版信息

J Bacteriol. 1968 Dec;96(6):2066-76. doi: 10.1128/jb.96.6.2066-2076.1968.

Abstract

The relationships between macromolecular synthesis and viability have been studied in the pleuropneumonia-like organism Mycoplasma laidlawii B adapted to a semidefined grwoth medium. This organism exhibited an absolute growth requirement for the nucleosides uridine and thymidine, a partial requirement for guanosine and deoxyguanosine, but no requirement for adenosine, deoxyadenosine, cytosine, and deoxycytosine. Cytosine and deoxycytosine partially satisfied the requirement for uridine. Loss in viability resulted from thymidine deprivation, but not from a deficiency in other growth requirements. This phenomenon of thymineless death in a mycoplasma is similar in many respects to that reported in other bacterial systems. Chloramphenicol specifically inhibited protein synthesis and allowed deoxyribonucleic acid synthesis to proceed to only about 40% of that normally produced per generation period, while causing less inhibition of ribonucleic acid synthesis. Protein synthesis inhibition permitted thymineless death to a survival level of less than 0.5%, but ribonucleic acid synthesis inhibition resulted in a higher (10%) survival level. These results are consistent with previously noted aspects of thymineless death in Escherichia coli strains, which suggest that thymineless death is coupled to ribonucleic acid synthesis.

摘要

在适应半限定生长培养基的类胸膜肺炎微生物莱氏无胆甾原体B中,研究了大分子合成与生存能力之间的关系。该微生物对核苷尿苷和胸苷表现出绝对的生长需求,对鸟苷和脱氧鸟苷有部分需求,但对腺苷、脱氧腺苷、胞嘧啶和脱氧胞嘧啶无需求。胞嘧啶和脱氧胞嘧啶部分满足了对尿苷的需求。生存能力的丧失是由胸苷剥夺导致的,而不是由其他生长需求的缺乏引起的。支原体中这种无胸腺死亡现象在许多方面与其他细菌系统中报道的情况相似。氯霉素特异性抑制蛋白质合成,使脱氧核糖核酸合成仅进行到每个世代正常产生量的约40%,同时对核糖核酸合成的抑制较小。蛋白质合成抑制使无胸腺死亡后的存活水平低于0.5%,但核糖核酸合成抑制导致更高(10%)的存活水平。这些结果与先前在大肠杆菌菌株中无胸腺死亡的相关情况一致,这表明无胸腺死亡与核糖核酸合成相关。

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