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首页> 外文期刊>Journal of Virology >Genetics and Physiology of Bacteriophage T4 3′-Phosphatase: Evidence for Involvement of the Enzyme in T4 DNA Metabolism
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Genetics and Physiology of Bacteriophage T4 3′-Phosphatase: Evidence for Involvement of the Enzyme in T4 DNA Metabolism

机译：噬菌体T4-磷酸酶的遗传和生理学：酶参与T4 DNA代谢的证据

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摘要

Mutants of bacteriophage T4D which fail to induce the deoxyribonucleotide-specific T4 3′-phosphatase have been isolated. These mutants (T4pseT) grow as well as wild-type T4 in most strains of Escherichia coli, but not in the T4-sensitive “Hospital Strain,” CT196, or in a derivative strain, CTr5x. Both the formation of infectious centers and the final yield of phage are reduced by 98% when CTr5x is infected by T4pseT mutants. The growth defects are accompanied by a 50% reduction in the rate of T4 DNA synthesis, a decrease in the single-strand length of the DNA product to about one-half the mature length, and greatly reduced packaging of DNA into phage particles. Introduction of an extra-cistronic suppressor mutation (stp) into T4pseT eliminates both the requirement for the T4 3′-phosphatase in infected CTr5x and the other observed effects of the pseT mutations. The pseT gene lies between genes 63 and 31. The stp gene lies in the nonessential region between rIIB and ac. Our results suggest that 3′-phosphoryl termini can disrupt T4 DNA replication to the extent that T4 3′-phosphatase becomes required for phage production.
机译：未诱导脱氧核糖核苷酸特异性T4 3'-磷酸酶的噬菌体T4D的突变体已被分离出来。这些突变体（t4 pset ）在大多数大肠杆菌Coli 的菌株中生长，但不是在T4敏感的“医院菌株”，CT196或在衍生菌株中，CTR5x。当CTR5X感染T4 PSET 突变体时，传染性中心的形成和噬菌体的最终产率降低了98％。生长缺陷伴随着T4 DNA合成率降低50％，DNA产物的单链长度的降低至成熟长度约为一半，并大大将DNA包装成噬菌体颗粒。将超声抑制突变（ STP ）引入T4 Pset 中，消除了感染的CTR5x中T4 3'-磷酸酶的要求和 pset 突变。 pset 基因位于113和31之间。 stp 基因位于 R IIB和 AC之间的非必要区域。我们的结果表明，3'-磷素末端可以破坏T4 DNA复制在噬菌体生产所需的T4 3'-磷酸酶的程度上。

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