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首页> 外文期刊>Journal of Virology >Breakdown and Exclusion of Superinfecting T-Even Bacteriophage in Escherichia coli
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Breakdown and Exclusion of Superinfecting T-Even Bacteriophage in Escherichia coli

机译:在大肠杆菌中击穿和排除超育t-oven噬菌体

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摘要

In bacterial strains containing the deoxyribonuclease endonuclease I (endonuclease I+ strains), 70 to 80% of the injected superinfecting T-even phage deoxyribonucleic acid (DNA) is rapidly degraded to oligonucleotides having an average chain length of 8, the same value as that obtained by endonuclease I digestion of purified T-even phage DNA in vitro. In endonuclease I? strains, less than 5% of the injected superinfecting T-even phage DNA is degraded to acid-soluble components. The superinfecting phage DNA is, however, fragmented into a large segment having a molecular weight of about 90 × 106 and 30 or more small acid-insoluble segments having molecular weights of less than 106. In both endonuclease I+ and endonuclease I? strains, over 80% of the DNA from adsorbed primary T2 or T4 phage, but only 50% of the DNA from adsorbed superinfecting T2 or T4 phage, is injected. Superinfecting T4 are genetically excluded as efficiently from endonuclease I? strains as they are from endonuclease I+ strains. The excluded phage cannot complement defects in either early or late gene functions carried by the primary phage. The induction of both superinfection breakdown and superinfection exclusion requires a period of protein synthesis between primary infection and addition of the superinfecting phage. These observations seem best explained by failure of superinfecting DNA to enter the host cell cytoplasm, presumably as a result of changes in the cell envelope induced by the primary phage.
机译:在含有脱氧核酸核酸酶内切核酸酶I的细菌菌株(内切酶I + 菌株)中,70至80%的注射的超胶片T-偶数脱氧核糖核酸(DNA)迅速降解到具有平均链长的寡核苷酸参照图8,与内切核酸酶I获得的值相同的值,i含有纯化的T-甚至噬菌体DNA在体外消化。在内切核酸酶I β菌株中,少于5%的注射的超细化T-偶数DNA降解到酸溶性组分中。然而,超细化噬菌体DNA是将分子量为约90×10 6℃的大的段,其分子量为小于10 6的分子量为约90×10 和30个或更多个小酸不溶性区段。在内切核酸酶中,I + 和内切核酸酶I β-β-菌株,来自吸附的伯t2或t4噬菌体的80%的DNA,但仅50%的DNA来自吸附的超键fecting t2或T4噬菌体注射。基因上的Superfectizing T4在核酸内核酸酶I α菌株中被遗传排除,因为它们来自内切核酸酶I + / sup>菌株。排除的噬菌体不能在初级噬菌体携带的早期或晚期基因功能中补充缺陷。 SuperInfection崩溃和超素排斥的诱导需要初级感染之间的蛋白质合成,并加入超细噬菌体。这些观察结果似乎最好通过失败的DNA进入宿主细胞质来解释,这可能是由于初级噬菌体诱导的细胞包络的变化导致。

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