Warner H R, Demple B F, Deutsch W A, Kane C M, Linn S
Proc Natl Acad Sci U S A. 1980 Aug;77(8):4602-6. doi: 10.1073/pnas.77.8.4602.
The characteristics of the nicks (single-strand breaks) introduced into damaged DNA by Escherichia coli endonucleases III, IV, and VI and by phage T4 UV endonuclease have been investigated with E. coli DNA polymerase I (DNA nucleotidyltransferase). Nicks introduced into depurinated DNA by endonuclease IV or VI provide good primer termini for the polymerase, whereas nicks introduced into depurinated DNA by endonuclease III or into irradiated DNA by T4 UV endonuclease do not. This result suggests that endonuclease IV nicks depurinated DNA on the 5' side of the apurinic site, as does endonuclease VI, whereas endonuclease III has a different incision mechanism. T4 UV endonuclease also possesses apurinic endonuclease activity that generates nicks in depurinated DNA with low priming activity for the polymerase. The priming activity of DNA nicked with endonuclease III or T4 UV endonuclease can be enhanced by an additional incubation with endonuclease VI and, to a lesser extent, by incubation with endonuclease IV. These results indicate that endonuclease III and T4 UV endonuclease (acting upon depurinated and irradiated DNA, respectively) generate nicks containing apurinic/apyrimidinic sites at their 3' termini and that such sites are not rapidly excised by the 3' leads to 5' activity of DNA polymerase I. However, endonuclease IV or VI apparently can remove such terminal apurinic/apyrimidinic sites as well as cleave on the 5' side of the unnicked sites. These results suggest roles for endonucleases III, IV, and VI in the repair of apurinic/apyrimidinic sites as well as pyrimidine dimer sites in DNA. Our results with T4 UV endonuclease suggest that the incision of irradiated DNA by T4 UV endonuclease involves both cleavage of the glycosylic bond at the 5' half of the pyrimidine dimer and cleavage of the phosphodiester bond originally linking the two nucleotides of the dimer. They also imply that the glycosylic bond is cleaved before the phosphodiester bond.
利用大肠杆菌DNA聚合酶I(DNA核苷酸转移酶),对大肠杆菌核酸内切酶III、IV和VI以及噬菌体T4紫外线核酸内切酶在受损DNA中引入的切口(单链断裂)的特征进行了研究。核酸内切酶IV或VI在脱嘌呤DNA中引入的切口为聚合酶提供了良好的引物末端,而核酸内切酶III在脱嘌呤DNA中引入的切口或T4紫外线核酸内切酶在经辐射的DNA中引入的切口则不然。这一结果表明,核酸内切酶IV与核酸内切酶VI一样,在脱嘌呤位点的5'侧切割脱嘌呤DNA,而核酸内切酶III具有不同的切割机制。T4紫外线核酸内切酶也具有脱嘌呤核酸内切酶活性,它在脱嘌呤DNA中产生的切口对聚合酶的引发活性较低。用核酸内切酶III或T4紫外线核酸内切酶切割的DNA的引发活性可通过与核酸内切酶VI的额外孵育得到增强,在较小程度上也可通过与核酸内切酶IV的孵育得到增强。这些结果表明,核酸内切酶III和T4紫外线核酸内切酶(分别作用于脱嘌呤和经辐射的DNA)在其3'末端产生含有脱嘌呤/脱嘧啶位点的切口,并且DNA聚合酶I的3'至5'活性不会迅速切除这些位点。然而,核酸内切酶IV或VI显然可以去除这种末端的脱嘌呤/脱嘧啶位点,并在未切割位点的5'侧进行切割。这些结果表明核酸内切酶III、IV和VI在DNA中脱嘌呤/脱嘧啶位点以及嘧啶二聚体位点的修复中发挥作用。我们对T4紫外线核酸内切酶的研究结果表明,T4紫外线核酸内切酶对经辐射的DNA的切割涉及嘧啶二聚体5'半部分的糖苷键断裂以及最初连接二聚体两个核苷酸的磷酸二酯键断裂。它们还暗示糖苷键在磷酸二酯键之前断裂。