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噬菌体T4中的热诱变:沿着颠换途径的又一次探索。

Heat mutagenesis in bacteriophage T4: another walk down the transversion pathway.

作者信息

Kricker M C, Drake J W

机构信息

Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.

出版信息

J Bacteriol. 1990 Jun;172(6):3037-9. doi: 10.1128/jb.172.6.3037-3039.1990.

Abstract

Extracellular nonreplicating bacteriophage T4 particles accumulate mutations as functions of temperature, time, pH, and ionic environment via two mechanisms: 5-hydroxymethylcytidine deamination produces G.C----A.T transitions while a guanosine modification produces transversions. Neither frameshift mutations nor mutations at A.T base pairs are appreciably induced. We now show that heat induces G.C----T.A transversions which we suggest may arise via a G*.A mispair, in which G* is a modified guanosine that has experienced a glycosylic bond migration. The rate of this reaction at 37 degrees C is sufficient to present a genetic hazard, particularly to large genomes; thus, the lesion is probably efficiently repaired in cellular genomes.

摘要

细胞外非复制性噬菌体T4颗粒通过两种机制随温度、时间、pH值和离子环境积累突变:5-羟甲基胞嘧啶脱氨产生G.C到A.T的转换,而鸟苷修饰产生颠换。移码突变和A.T碱基对处的突变均未明显诱导产生。我们现在表明,热诱导G.C到T.A的颠换,我们认为这可能是通过G*.A错配产生的,其中G*是经历了糖苷键迁移的修饰鸟苷。该反应在37摄氏度时的速率足以构成遗传危害,尤其是对大基因组而言;因此,这种损伤可能在细胞基因组中得到有效修复。

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