INDUCTION OF BASE SUBSTITUTION MUTATIONS BY AFLATOXIN-B1 IS MUCAB DEPENDENT IN ESCHERICHIA-COLI
INDUCTION OF BASE SUBSTITUTION MUTATIONS BY AFLATOXIN-B1 IS MUCAB DEPENDENT IN ESCHERICHIA-COLI
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DOI：
10.1128/jb.170.8.3415-3420.1988
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发表时间：
1988-08-01
影响因子：
3.2
通讯作者：
EISENSTADT, E
中科院分区：
文献类型：
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作者：
FOSTER, PL;GROOPMAN, JD;EISENSTADT, E
大肠杆菌中黄曲霉毒素B1诱导的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;大肠杆菌类似物。umuDC+是不够的。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。无论是预诱导的SOS反应，也不存在额外的拷贝umuDC+允许恢复黄曲霉毒素B1诱导的碱基置换。因此，由黄曲霉毒素B1诱导的预诱变DNA损伤揭示了UmuDC和MucAB之间的功能差异。我们估计，在MucAB的存在下，黄曲霉毒素B1诱导的DNA损伤将转化为突变的概率增加至少10倍。
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 premutagentic 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.