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5-碘尿嘧啶在无光条件下对噬菌体T4td8生长和生物合成过程的影响。

The effect of 5-iodouracil on the growth and biosynthetic processes of bacteriophage T4td8 in the absence of light.

作者信息

Byrd D M, Prusoff W H

出版信息

Chem Biol Interact. 1976 Feb;12(2):197-210. doi: 10.1016/0009-2797(76)90099-5.

DOI:10.1016/0009-2797(76)90099-5
PMID:764990
Abstract

5-Iodouracil (IUra)-substituted progeny bacteriophage T4td8 were grown under conditions such that, upon CsCl equilibrium isopycnic gradient centrifugation, progeny with density distributions about the median similar to that of unsubstituted phage are obtained. In the absence of light a monotonic relationship exists between decreasing progeny viability and increasing percent IUra substitution. IUra is equivalent to thymine as a growth factor on a molar basis, and at concentrations of IUra plus thymine above that required for maximum particle production, the percent IUra substitution in phage DNA is determined by the mole fraction of IUra in the medium. The lethal effects of 5-iodo-2'-deoxyuridine (IdUrd) and IUra are equivalent, and are not produced by a direct effect on the phage particles. At equivalent percent substitution in phage DNA the order of lethality is IUra greater than 5-bromouracil (BrUra) greater than 5-chlorouracil (ClUra). There is no interference with the transfer of thymine from host cell to progeny phage by the presence of IUra in the medium, and IUra affects neither the time of lysis nor the content of phage DNA in the infected cells.

摘要

5-碘尿嘧啶(IUra)取代的子代噬菌体T4td8在这样的条件下生长:经CsCl平衡等密度梯度离心后,可获得密度分布在中位数附近且与未取代噬菌体相似的子代。在无光条件下,子代活力降低与IUra取代百分比增加之间存在单调关系。IUra在摩尔基础上作为生长因子等同于胸腺嘧啶,并且在IUra加胸腺嘧啶的浓度高于最大颗粒产生所需浓度时,噬菌体DNA中IUra的取代百分比由培养基中IUra的摩尔分数决定。5-碘-2'-脱氧尿苷(IdUrd)和IUra的致死效应相同,且不是由对噬菌体颗粒的直接作用产生的。在噬菌体DNA中取代百分比相等时,致死顺序为IUra大于5-溴尿嘧啶(BrUra)大于5-氯尿嘧啶(ClUra)。培养基中存在IUra不会干扰胸腺嘧啶从宿主细胞向子代噬菌体的转移,并且IUra既不影响裂解时间也不影响感染细胞中噬菌体DNA的含量。

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引用本文的文献

1
Lethal and mutagenic effects of 5-iodouracil on bacteriophage T4td8rII.5-碘尿嘧啶对噬菌体T4td8rII的致死和诱变作用。
Antimicrob Agents Chemother. 1977 Feb;11(2):312-7. doi: 10.1128/AAC.11.2.312.