黄曲霉毒素B1诱导的碱基替换突变在大肠杆菌中依赖于mucAB。
Induction of base substitution mutations by aflatoxin B1 is mucAB dependent in Escherichia coli.
作者信息
Foster P L, Groopman J D, Eisenstadt E
机构信息
Division of Environmental Health, Boston University School of Public Health, Massachusetts 02118.
出版信息
J Bacteriol. 1988 Aug;170(8):3415-20. doi: 10.1128/jb.170.8.3415-3420.1988.
Abstract
Recovery of aflatoxin B1-induced base substitution mutations in Escherichia coli was almost completely dependent on the presence of the SOS-mutagenesis-enhancing operon mucAB+; the normal E. coli analog, umuDC+, was not sufficient. Yet aflatoxin B1 induced the SOS response, including the umuDC operon, as well as did UV light. Neither preinduction of the SOS response nor the presence of additional copies of umuDC+ allowed the recovery of aflatoxin B1-induced base substitutions. Thus, the premutagenic DNA lesions induced by aflatoxin B1 reveal a functional difference between UmuDC and MucAB. We estimate that in the presence of MucAB the probability that aflatoxin B1-induced DNA lesions will be converted into mutations is increased at least 10-fold.
摘要
黄曲霉毒素B1诱导的大肠杆菌碱基置换突变的恢复几乎完全依赖于SOS诱变增强操纵子mucAB+的存在；正常的大肠杆菌类似物umuDC+并不足够。然而，黄曲霉毒素B1诱导了SOS反应，包括umuDC操纵子，紫外线也是如此。SOS反应的预诱导或umuDC+额外拷贝的存在都不能使黄曲霉毒素B1诱导的碱基置换得以恢复。因此，黄曲霉毒素B1诱导的诱变前DNA损伤揭示了UmuDC和MucAB之间的功能差异。我们估计，在存在MucAB的情况下，黄曲霉毒素B1诱导的DNA损伤转化为突变的概率至少增加10倍。
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