大肠杆菌中作为SOS活性的Tn5切除与转座
Excision and transposition of Tn5 as an SOS activity in Escherichia coli.
作者信息
Kuan C T, Liu S K, Tessman I
机构信息
Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907.
出版信息
Genetics. 1991 May;128(1):45-57. doi: 10.1093/genetics/128.1.45.
Excision and transposition of the Tn5 element in Escherichia coli ordinarily appear to occur by recA-independent mechanisms. However, recA(Prtc) genes, which encode RecA proteins that are constitutively activated to the protease state, greatly enhanced excision and transposition; both events appeared to occur concomitantly and without destruction of the donor DNA. The recombinase function of the RecA protein was not required. Transposition was accompanied by partial, and occasionally full, restoration of the functional integrity of the gene vacated by the excised Tn5. The stimulation of transposition was inhibited by an uncleavable LexA protein and was strongly enhanced by an additional role of the RecA(Prtc) protein besides its mediation of LexA cleavage. To account for the enhanced transposition, we suggest that (i) there may be a LexA binding site within the promoter for the IS50 transposase, (ii) activated RecA may cleave the IS50 transposition inhibitor, and (iii) the transposase may be formed by RecA cleavage of a precursor molecule.
在大肠杆菌中，Tn5 元件的切除和转座通常似乎是通过不依赖 recA 的机制发生的。然而，recA(Prtc) 基因编码的 RecA 蛋白持续激活至蛋白酶状态，极大地增强了切除和转座；这两个事件似乎同时发生，且供体 DNA 未被破坏。RecA 蛋白的重组酶功能并非必需。转座伴随着被切除的 Tn5 腾出的基因功能完整性的部分恢复，偶尔会完全恢复。转座的刺激被不可切割的 LexA 蛋白抑制，并且除了介导 LexA 切割外，RecA(Prtc) 蛋白的额外作用使其强烈增强。为了解释转座增强的现象，我们认为：(i) IS50 转座酶的启动子内可能存在一个 LexA 结合位点；(ii) 激活的 RecA 可能切割 IS50 转座抑制物；(iii) 转座酶可能由 RecA 对前体分子的切割形成。
Zotero 插件