首页> 外文期刊>Journal of Virology >F-Factor-mediated restriction of bacteriophage T7: protein synthesis in cell-free systems from T7-infected Escherichia coli F- and F+ cells.
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F-Factor-mediated restriction of bacteriophage T7: protein synthesis in cell-free systems from T7-infected Escherichia coli F- and F+ cells.

机译:F因子介导的噬菌体T7的限制:来自T7感染大肠杆菌F和F +细胞的无细胞系统中的蛋白质合成。

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A characteristic phenomenon in the F-factor-mediated inhibition of T7 phage is a virtual absence of T7 late protein synthesis in T7-infected Escherichia coli male cells, in spite of the presence of T7 late mRNA which is translatable in vitro when isolated from the cell. To determine whether the translational defect in T7-infected F+ cells is due to a T7 late mRNA-specific translational block, or to a general decrease of F+ cell translational activity, we compared the activities of cell-free, protein-synthesizing systems prepared from isogenic F- and F+ cells harvested at different times of T7 infection. The cell-free systems from uninfected F- and F+ cells translated T7late mRNA equally as well as MS2 RNA and T7early mRNA. The activity of cell-free systems from T7-infected F+ cells to translate MS2 RAN, T7 early mRNA, and T7 late mRNA decreased concomitantly at a much faster rate than that of T7-infected F- cells. Therefore, the abortive infection of F+ cells by T7 does not result from a T7 late mRNA-specific translational inhibition, although a general reduction of the translational activity appears to be a major factor for the inability of the F+ cells to produce a sufficient amount of T7 late proteins.
机译:F因子介导的T7噬菌体抑制的特征现象是T7感染大肠杆菌雄性细胞中的虚拟不存在T7晚期蛋白质合成,尽管存在T7晚mRNA,其在从中分离出细胞。为了确定T7感染的F +细胞中的翻译缺陷是否是由于T7晚期mRNA特异性转化块,或者对F +细胞翻译活动的一般降低,我们比较了由此制备的无细胞,蛋白质合成系统的活性在T7感染的不同时间收获的同种型F +细胞。从未感染的F +细胞和F +细胞的无细胞系统平均平均T7late mRNA以及MS2 RNA和T3Sly mRNA。来自T7感染的F +细胞的无细胞系统的活性以翻译MS2 RAN,T7早期mRNA和T7晚期mRNA以比T7感染的F细胞的速度更快地降低。因此,T7对F +细胞的流入感染不会由T7晚期mRNA特异性平移抑制产生,尽管翻译活动的一般减少似乎是F +细胞产生足够量的主要因素T7晚期蛋白质。

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  • 来源
    《Journal of Virology》 |1975年第6期|共9页
  • 作者

    Y Yamada; D Nakada;

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  • 收录信息 美国《科学引文索引》(SCI);
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