Walker G C, Marsh L, Dodson L
Environ Health Perspect. 1985 Oct;62:115-7. doi: 10.1289/ehp.8562115.
For many years, the study of the regulation of the SOS network was complicated by both the complexities of the responses and the interrelationships of the key regulatory elements. However, recently the application of powerful genetic and molecular biological techniques has allowed us to gain a detailed picture of the regulation of this complex network. The network is now known to consist of more than 17 genes, each of which is repressed by the LexA protein. Induction of the genes in the SOS network occurs when the RecA protein becomes activated in response to a signal generated by DNA damage. Two of the genes in this network, umuD and umuC, are absolutely required for mutagenesis by UV and various carcinogens. The umuD and umuC genes have molecular weights of 16,000 and 45,000 daltons, respectively, and are organized in an operon repressed by LexA. The mutagenesis-enhancing plasmid pKM101 carries two genes mucA and mucB, which are analogs of the umuD and umuC genes, respectively.
多年来,SOS网络调控的研究因反应的复杂性以及关键调控元件之间的相互关系而变得复杂。然而,最近强大的遗传学和分子生物学技术的应用使我们能够详细了解这个复杂网络的调控情况。现在已知该网络由17个以上的基因组成,每个基因都受到LexA蛋白的抑制。当RecA蛋白响应DNA损伤产生的信号而被激活时,SOS网络中的基因就会被诱导表达。该网络中的两个基因umuD和umuC是紫外线和各种致癌物诱变所绝对必需的。umuD和umuC基因的分子量分别为16,000和45,000道尔顿,并以一个受LexA抑制的操纵子形式存在。诱变增强质粒pKM101携带两个基因mucA和mucB,它们分别是umuD和umuC基因的类似物。