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首页> 外文期刊>Journal of Virology >Bacteriophage T4 Inhibits Colicin E2-Induced Degradation of Escherichia coli Deoxyribonucleic Acid II. Inhibition by T4 Ghosts and by T4 in the Absence of Protein Synthesis
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Bacteriophage T4 Inhibits Colicin E2-Induced Degradation of Escherichia coli Deoxyribonucleic Acid II. Inhibition by T4 Ghosts and by T4 in the Absence of Protein Synthesis

机译：噬菌体T4抑制耐植物E2诱导的大肠杆菌脱氧核糖核酸II的降解。在没有蛋白质合成的情况下，T4鬼魂和T4抑制

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The deoxyribonucleic acid (DNA) of Escherichia coli B is converted by colicin E2 to products soluble in cold trichloroacetic acid; we showed previously that this DNA degradation (hereafter termed solubilization) is subject to inhibition by infection with phage T4 and that at least two modes of inhibition can be differentiated on the basis of their sensitivity to chloramphenicol (CM). This report deals exclusively with the inhibition of E2 produced by T4, or T4 ghosts, in the absence of protein synthesis. The following observations are described. (i) The stage of T4 infection that inhibits E2 occurs after reversible adsorption of the phage to the bacterial surface, but probably prior to injection of T4 DNA into the cell's interior. (ii) The extent of inhibition increases as the T4 multiplicity is increased; however, the fraction of bacterial DNA that eventually is solubilized is virtually independent of the phage multiplicity. (iii) Phage ghosts (DNA-less phage particles) possess an approximately 15-fold greater inhibitory capacity toward E2 than do intact phage; however, because highly purified T4 (completely freed of ghost contamination) still inhibit E2, we discount the possibility that preparations of “intact phage” inhibit exclusively by virtue of contaminating ghosts. (iv) T4 infection does not liberate an extracellular inactivator of E2. In fact, infection with sufficiently high multiplicities of T4 produces a supernatant factor that protects E2 from nonspecific inactivation at 37 C. This protective factor does not interfere with the colicin's ability to induce DNA solubilization. (v) Inhibition of E2 occurs even when phage are added well after initiation of DNA solubilization by E2, suggesting that a late stage of E2 action is the target of inhibition by T4 infection. (vi) Increasing the CM concentration from 50 μg/ml to 200 μg/ml appears to reduce the inhibition appreciably; however, this can be attributed to an enhancement by CM of the rate of E2-induced DNA solubilization. (vii) The same degree of inhibition of E2 by T4 seen in CM is observed when CM is replaced by puromycin or rifampin. (viii) Others have shown that raising the multiplicity of E2 increases the rate of DNA solubilization. We find that the fractional inhibition (i), [i = (1 ? yi/yo), where yi and yo represent the inhibited and uninhibited rates of solubilization of DNA, respectively], produced by a given T4 multiplicity is independent of the multiplicity of E2 and hence is independent of the rate of DNA solubilization induced by E2.
机译：大肠杆菌Coli B的脱氧核糖核酸（DNA）由肠E2转化为溶于冷三氯乙酸的产物;我们以前表明该DNA降解（下文称为溶解）通过用噬菌体T4感染而受到抑制，并且可以基于它们对氯霉素（cm）的敏感性来区分至少两种抑制模式。本报告仅涉及在没有蛋白质合成的情况下抑制T4或T4鬼魂产生的E2。描述了以下观察结果。 （i）抑制E2的T4感染的阶段在可逆吸附噬菌体至细菌表面之后发生，但可能在将T4 DNA注入细胞内部之前。 （ii）随着T4多重性增加，抑制程度增加;然而，最终溶解的细菌DNA的分数实际上与噬菌体多重相比。 （III）噬菌体鬼（DNA-噬菌体颗粒）具有比完整的噬菌体更高的抑制能力大约15倍。然而，由于高度纯化的T4（完全排出鬼魂污染）仍然抑制E2，我们遵循凭借污染鬼魂的“完整噬菌体”抑制的可能性折扣。 （iv）T4感染不能释放E2的细胞外灭菌剂。实际上，具有足够高的T4多重性的感染产生了37℃的非特异性灭活的上清液因子。这种保护因子不会干扰肠道诱导DNA溶解的能力。 （v）即使在通过E2开始DNA溶解后加入良好的噬菌体，表明E2动作的后期是T4感染的目标，也会发生E2的抑制。 （VI）将CM浓度从50μg/ ml增加到200μg/ mL，似乎显着降低抑制;然而，这可以归因于CM的E2诱导的DNA溶解速率的增强。 （vii）当CM被嘌呤霉素或利福平蛋白代替时，观察到在CM中看到的T4的抑制程度相同的抑制。 （VIII）其他表明提高了多种E2增加了DNA溶解的速率。我们发现分数抑制（i），[i =（1？y i / y o ），其中Y i 和y < Sub> O 代表DNA的抑制和未抑制的DNA溶解率），通过给定的T4多重性产生与E2的多重性无关，因此与E2诱导的DNA溶解速率无关。

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