Thermal resistance to photoreactivation of specific mutations potentiated in E. coli B/r ung by ultraviolet light

Thermal resistance to photoreactivation of specific mutations potentiated in E. coli B/r ung by ultraviolet light
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紫外线增强大肠杆菌 B/r ung 中特定突变的热抗性

DOI:
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发表时间:
2004
期刊:
Molecular and General Genetics MGG
影响因子:
--
通讯作者:
R. Bockrath
R. Bockrath
中科院分区:
--
文献类型:
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作者:
D. Fix;R. Bockrath

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本研究采用紫外线对一株大肠杆菌进行诱变。coli ung,其缺乏尿嘧啶-DNA糖基化酶活性。在已经由萘啶酸处理诱导的细胞中由UV增强的突变仍然是光可逆的,这表明嘧啶二聚体直接作为预突变光产物。其次,将经照射的细胞在48°C下保持在缓冲液中0至135分钟以允许嘧啶二聚体中的胞嘧啶脱氨基。在光复活之前和之后,作为这种热处理的函数,单独确定2类从头抑制突变、2类转换抑制突变和回复突变的突变频率。回复突变在整个治疗过程中对光复活敏感,但从头突变和转换的抑制突变迅速产生了对光复活的抗性。在ung+对照中未观察到这种抗性。提出了一个模型来解释选择性耐药的基础上的假设,即2类从头和转换抑制突变通常导致UV GC到AT转换在T=C二聚体。该模型描述了这些二聚体中胞嘧啶残基的脱氨基作用,成为尿嘧啶残基。因此,在不能修复DNA中尿嘧啶的细胞中通过光复活的单体化不再逆转突变,并且在尿嘧啶位点建立GC至AT的转换。
SummaryMutagenesis by ultraviolet light was studied in a strain of E. coli ung, which lacks uracil-DNA glycosylase activity. Mutation potentiated by UV in cells already induced by nalidixic acid treatment was still photoreversible suggesting that pyrimidine dimers act directly as premutational photoproducts. Secondly, irradiated cells were held in buffer at 48°C for 0 to 135 min to allow for deamination of cytosines in pyrimidine dimers. The mutation frequencies for class 2 de novo suppressor mutation, for class 2 converted suppressor mutation and for backmutation were individually determined, before and after photoreactivation, as a function of this thermal treatment. Backmutation remained sensitive to photoreactivation throughout the treatment but de novo and converted suppressor mutations rapidly developed resistance to photoreactivation. This resistance was not seen in an ung+ control. A model is proposed to account for the selective resistance based on the hypothesis that class 2 de novo and converted suppressor mutations normally result from UV by GC to AT transitions at T=C dimers. The model describes deamination of the cytosine residues in these dimers to become uracil residues. In consequence, monomerization by photoreactivation in cells that can not repair uracils in DNA no longer reverses mutation and GC to AT transitions are established at the sites of uracils.
大肠杆菌中紫外线诱变的拥挤抑制。
DOI: 10.1016/0027-5107(80)90134-7
发表时间: 1980
期刊: Mutation research
影响因子: --
作者:
Bockrath,R;Harper,D;Kristoff,S
通讯作者: Kristoff,S