The role of SOS and flap processing in microsatellite instability in Escherichia coli
The role of SOS and flap processing in microsatellite instability in Escherichia coli
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DOI：
10.1073/pnas.95.17.10003
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发表时间：
1998-08-18
影响因子：
11.1
通讯作者：
Cassuto, E
中科院分区：
文献类型：
--
作者：
Morel, P;Reverdy, C;Cassuto, E
影响错配修复的突变会导致原核生物和真核生物中微卫星长度改变的频率增加，然而，发现在具有功能错配修复系统的细胞中经常发现微卫星不稳定，促使人们寻找其他导致轨道改变的因素。在本报告中，我们表明，在大肠杆菌中，聚(AC/TG)链因诱导SOS的突变而不稳定。这些观察结果可能对真核细胞有影响，因为最近的结果表明，哺乳动物存在类似于原核生物的SOS反应，此外，与哺乳动物FEN1和酵母RAD27核酸酶同源的DNA聚合酶I的5‘-3’外切酶区域的缺陷导致了几种遗传疾病特征的重复扩张显著增加，最后，我们发现校对缺陷和错配修复缺陷的组合导致了极端的微卫星不稳定性。
Mutations affecting mismatch repair result in elevated frequencies of microsatellite length alteration in prokaryotes and eukaryotes, However, the finding that microsatellite instability is found often in cells with a functional mismatch repair system prompted a search for other factors of tract alteration. In the present report, we show that, in Escherichia coli, poly(AC/TG) tracts are destabilized by mutations that induce SOS. These observations may have implications for eukaryotic cells because recent results suggest the existence of a mammalian SOS response analogous to that in prokaryotes, In addition, a defect in the 5'-3' exonuclease domain of DNA polymerase I, homologous to the mammalian FEN1 and the yeast RAD27 nucleases, leads to a marked increase in repeat expansions characteristic of several genetic disorders, Finally, we found that the combination of a proofreading defect with mismatch repair deficiency results in extreme microsatellite instability.