Janel-Bintz R, Maenhaut-Michel G, Fuchs R P
Cancérogenèse et Mutagenèse Molèculaire et Structurale, UPR 9003 CNRS, Pôle API ESBS, Illkirch, France.
Mol Gen Genet. 1994 Nov 1;245(3):279-85. doi: 10.1007/BF00290107.
N-2-acetylaminofluorene has been shown efficiently to induce both -1 and -2 frameshift mutations in Escherichia coli as well as in mammalian cells. In E. coli, the genetic characteristics of -1 and -2 frameshift mutations were found to be distinct. The -1 frameshift mutation pathway occurs at monotonous runs of G residues (i.e. GGG-->GG). This pathway exhibits the same genetic requirements as UV light-induced base substitution mutagenesis. Indeed, optimal mutagenesis requires the expression of both UmuDC and the activated form of RecA. The -2 frameshift mutation pathway operates at short alternating GpC sequences, such as the NarI sequence (i.e. GGCGCC-->GGCC). In contrast to the -1 frameshift mutation pathway, optimal induction does not require the UmuDC and RecA proteins. This pathway involves a LexA-repressed function tentatively called Npf (for NarI processing factor). In this paper, we show that MucAB efficiently stimulates the -2 frameshift mutation pathway. However, unlike the Npf pathway, MucAB-mediated stimulation requires expression of the RecA protein.
N-2-乙酰氨基芴已被证明能在大肠杆菌和哺乳动物细胞中高效诱导-1和-2移码突变。在大肠杆菌中，-1和-2移码突变的遗传特征被发现是不同的。-1移码突变途径发生在G残基的单调重复序列处（即GGG→GG）。该途径表现出与紫外线诱导的碱基替代诱变相同的遗传要求。实际上，最佳诱变需要UmuDC和RecA的活化形式的表达。-2移码突变途径在短的交替GpC序列处起作用，例如NarI序列（即GGCGCC→GGCC）。与-1移码突变途径相反，最佳诱导不需要UmuDC和RecA蛋白。该途径涉及一种LexA抑制的功能，暂时称为Npf（用于NarI加工因子）。在本文中，我们表明MucAB能有效刺激-2移码突变途径。然而，与Npf途径不同，MucAB介导的刺激需要RecA蛋白的表达。
