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噬菌体T4基因43突变体的诱变和抗诱变效应中的位点特异性和变异性。

Site specificity and variability in the mutator and antimutator effects of phage T4 gene 43 mutants.

作者信息

Ronen A, Halevy C, Kass N

出版信息

Genetics. 1978 Dec;90(4):647-57. doi: 10.1093/genetics/90.4.647.

Abstract

Spontaneous, 2-aminopurine- and 5-bromouracil-induced mutations at six rII nonsense codons were studied in phage T4 strains possessing wild-type and mutant gene 43 alleles. The mutation pathways studied included interconversions and reversions of nonsense codons. The tsCB87 allele, which specifies an antimutator DNA polymerase, reduced base-analogue-induced mutation frequencies along all pathways. However, GC base pairs were less affected than AT base pairs. The frequency of spontaneous UAA leads to UAG conversions was also reduced by tsCB87, but that of spontaneous UAA leads to UAG UGA conversions was often increased. Mutation in the presence of the mutator allele tsL56 was increased along all pathways, with no preference for either AT or GC base pairs. Mutation frequencies in the presence of the two mutant DNA polymerases were highly variable. A strong correlation was found between 2-aminopurine-induced mutation frequencies in ts+ tsCB87 phage along the reversion and UAA changed to UAG (but not UAA changed to UGA) pathways.

摘要

在具有野生型和突变型基因43等位基因的噬菌体T4菌株中,研究了六个rII无义密码子处的自发突变以及由2-氨基嘌呤和5-溴尿嘧啶诱导的突变。所研究的突变途径包括无义密码子的相互转换和回复突变。指定抗突变DNA聚合酶的tsCB87等位基因降低了所有途径中碱基类似物诱导的突变频率。然而,GC碱基对比AT碱基对受影响更小。tsCB87也降低了自发的UAA转换为UAG的频率,但自发的UAA转换为UAG和UGA的频率通常会增加。在存在诱变等位基因tsL56的情况下,所有途径的突变均增加,对AT或GC碱基对均无偏好。在两种突变DNA聚合酶存在的情况下,突变频率变化很大。在ts + tsCB87噬菌体中,沿着回复突变途径以及UAA转变为UAG(但不是UAA转变为UGA)途径,发现2-氨基嘌呤诱导的突变频率之间存在很强的相关性。

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本文引用的文献

2
Antimutagenic DNA polymerases of bacteriophage T4.噬菌体T4的抗诱变DNA聚合酶
Cold Spring Harb Symp Quant Biol. 1968;33:339-44. doi: 10.1101/sqb.1968.033.01.039.
3
On the role of DNA polymerase in base selection.论DNA聚合酶在碱基选择中的作用。
Cold Spring Harb Symp Quant Biol. 1966;31:693-7. doi: 10.1101/sqb.1966.031.01.088.
4
Neighbor effects in the mutation of ochre triplets in the T 4 rII gene.
Mutat Res. 1971 Oct;13(2):109-13. doi: 10.1016/0027-5107(71)90002-9.
9
An analysis of replication errors made by a defective T4 DNA polymerase.
Mol Gen Genet. 1972;117(1):60-71. doi: 10.1007/BF00268838.

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