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脑膜炎肺炎病原体感染对其L细胞宿主的脱氧核糖核酸和蛋白质合成的影响。

Effect of infection with the meningopneumonitis agent on deoxyribonucleic acid and protein synthesis by its L-cell host.

作者信息

Alexander J J

出版信息

J Bacteriol. 1969 Feb;97(2):653-7. doi: 10.1128/jb.97.2.653-657.1969.

Abstract

Cycloheximide, which had already been shown to inhibit protein synthesis in Earle's L cells (mouse fibroblasts) without having any effect on the multiplication or protein synthesis in Chlamydia psittaci (strain meningopneumonitis) infecting these host cells, also caused greater than 90% inhibition of deoxyribonucleic acid (DNA) synthesis in L cells after a 3-hr exposure to the drug. L cells infected with the meningopneumonitis agent and treated with cycloheximide were used to follow meningopneumonitis-specific DNA synthesis during intracellular growth of the parasite. The rate at which labeled precursors were incorporated into parasite DNA doubled every 2 hr. The effect of meningopneumonitis infection on L-cell DNA and protein synthesis was investigated in logarithmically growing and in stationary-phase (nondividing) populations of L cells. Host-specific DNA and protein synthesis appeared to be inhibited in infected L cells when compared with logarithmically growing control cells, whereas no inhibition was apparent when the comparison was made with stationary-phase control cells. The maximal amount of protein and DNA synthesis that occurred in meningopneumonitis-infected L cells was equal to the amount of DNA and protein synthesized in logarithmically growing, uninfected L cells. A possible explanation of these results is given.

摘要

放线菌酮已被证明能抑制Earle's L细胞(小鼠成纤维细胞)中的蛋白质合成,而对感染这些宿主细胞的鹦鹉热衣原体(脑膜肺炎菌株)的繁殖或蛋白质合成没有任何影响。在接触该药物3小时后,放线菌酮也导致L细胞中脱氧核糖核酸(DNA)合成受到超过90%的抑制。感染了脑膜肺炎病原体并用放线菌酮处理的L细胞被用于追踪寄生虫在细胞内生长期间脑膜肺炎特异性DNA的合成。标记前体掺入寄生虫DNA的速率每2小时增加一倍。在对数生长期和静止期(不分裂)的L细胞群体中,研究了脑膜肺炎感染对L细胞DNA和蛋白质合成的影响。与对数生长期的对照细胞相比,感染的L细胞中宿主特异性DNA和蛋白质合成似乎受到抑制,而与静止期对照细胞相比时,没有明显的抑制作用。脑膜肺炎感染的L细胞中发生的蛋白质和DNA合成的最大量与对数生长期、未感染的L细胞中合成的DNA和蛋白质的量相等。文中给出了这些结果的一种可能解释。

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