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连接酶缺陷型噬菌体T4。II. 生理学研究。

Ligase-defective bacteriophage T4. II. Physiological studies.

作者信息

Koch R E

出版信息

J Virol. 1973 Jan;11(1):41-5. doi: 10.1128/JVI.11.1.41-45.1973.

Abstract

The timing of the suppression of gene 30 (deoxyribonucleic acid ligase) mutations by rII mutations was studied by temperature shift-down experiments with a temperature-sensitive rII mutation. The rII function must remain inactivated for about 5 to 8 min at 37 C for suppression to occur, thus making suppression an early function. This result is in agreement with the timing of expression of other rII functions. A gene 30 defect can also be overcome by replacing the Na(+) cation in the growth medium with the Mg(2+) cation, a result similar to the relief of the lethality of rII mutations in lambda lysogens. Prior infection with bacteriophages T3 or T7, which produce their own deoxyribonucleic acid ligases, can also partially overcome the lethality of gene 30 mutations.

摘要

利用温度敏感型rII突变通过降温实验研究了rII突变对基因30(脱氧核糖核酸连接酶)突变的抑制时机。rII功能必须在37℃下保持失活约5至8分钟才能发生抑制,因此抑制是一种早期功能。该结果与其他rII功能的表达时机一致。用Mg(2+)阳离子替代生长培养基中的Na(+)阳离子也可以克服基因30缺陷,这一结果类似于λ溶原菌中rII突变致死性的缓解。预先感染产生自身脱氧核糖核酸连接酶的噬菌体T3或T7,也可以部分克服基因30突变的致死性。

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A mutation of T4B phage, which enhances suppression of ligase mutants with rII mutations.
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Mutants of T7 bacteriophage inhibited by lambda prophage.被λ原噬菌体抑制的T7噬菌体突变体。
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