大肠杆菌的光复活作用可逆转紫外线对umuC的诱导。
Photoreactivation of Escherichia coli reverses umuC induction by UV light.
作者信息
Brash D E, Haseltine W A
出版信息
J Bacteriol. 1985 Aug;163(2):460-3. doi: 10.1128/jb.163.2.460-463.1985.
Abstract
UV mutagenesis in Escherichia coli depends on the presence of a premutagenic lesion in DNA and on the induction of the umuCD gene product as part of the SOS response. Using operon fusions between the E. coli lacZ gene and the SOS genes umuC, uvrB, and dinD, we have affirmed the expected role of the cyclobutane pyrimidine dimer in inducing SOS gene transcription. In addition, we found that photoreactivation of cyclobutane pyrimidine dimers reversed umuC induction to the same extent as it reversed mutagenesis. Therefore, the photoreactivability of UV mutagenesis does not itself identify the cyclobutane pyrimidine dimer as the UV mutagenic lesion in E. coli.
摘要
大肠杆菌中的紫外线诱变依赖于DNA中诱变前损伤的存在以及作为SOS应答一部分的umuCD基因产物的诱导。利用大肠杆菌lacZ基因与SOS基因umuC、uvrB和dinD之间的操纵子融合，我们证实了环丁烷嘧啶二聚体在诱导SOS基因转录中的预期作用。此外，我们发现环丁烷嘧啶二聚体的光复活与诱变的逆转程度相同，它也能逆转umuC的诱导。因此，紫外线诱变的光复活能力本身并不能确定环丁烷嘧啶二聚体就是大肠杆菌中的紫外线诱病变异损伤。
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