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首页> 外文期刊>Biochemistry >Alpha-anomeric deoxynucleotides, anoxic products of ionizing radiation, are substrates for the endonuclease IV-type AP endonucleases.
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Alpha-anomeric deoxynucleotides, anoxic products of ionizing radiation, are substrates for the endonuclease IV-type AP endonucleases.

机译：α-异常脱氧核苷酸，电离辐射的缺氧产物，是用于内切核酸酶IV型AP内切核酸酶的底物。

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摘要

Alpha-anomeric 2'-deoxynucleosides (alphadN) are one of the products formed by ionizing radiation (IR) in DNA under anoxic conditions. Alpha-2'-deoxyadenosine (alphadA) and alpha-thymidine (alphaT) are not recognized by DNA glycosylases, and are likely removed by the alternative nucleotide incision repair (NIR) pathway. Indeed, it has been shown that alphadA is a substrate for the Escherichia coli Nfo and human Ape1 proteins. However, the repair pathway for removal of alphadA and other alphadN in yeast is unknown. Here we report that alphadA when present in DNA is recognized by the Saccharomyces cerevisiae Apn1 protein, a homologue of Nfo. Furthermore, alphaT is a substrate for Nfo and Apn1. Kinetic constants indicate that alphadA and alphaT are equally good substrates, as a tetrahydrofuranyl (THF) residue, for Nfo and Apn1. Using E. coli and S. cerevisiae cell-free extracts, we have further substantiated the role of the nfo and apn1 gene products in the repair of alphadN. Surprisingly, we found that bacteria and yeast NIR-deficient mutants are not sensitive to IR, suggesting that DNA strand breaks with terminal 3'-blocking groups rather than alphadN might contribute to cell survival. We propose that the novel substrate specificities of Nfo and Apn1 play an important role in counteracting oxidative DNA base damage.
机译：α-异常2'-脱氧核苷（alphadn）是通过在缺氧条件下的DNA中的电离辐射（IR）形成的产物之一。 DNA糖基酶不识别α-2'-脱氧腺苷（alphada）和α-胸苷（AlphaT），并且可能通过替代核苷酸切口修复（NIR）途径除去。实际上，已经表明，alphada是大肠杆菌NFO和人APE1蛋白的底物。然而，用于去除alphada和酵母中其他alphadn的修复途径是未知的。在这里，我们举报的是，当酿酒酵母酿酒酵母APN1蛋白识别DNA时，alphada被报告在DNA中，NFO的同源物识别。此外，α是NFO和APN1的底物。动力学常数表明，α和α是同等良好的底物，作为NFO和APN1的四氢呋喃基（THF）残余物。使用大肠杆菌和酿酒酵母无细胞提取物，我们进一步证实了NFO和APN1基因产物在Alphadn修复中的作用。令人惊讶的是，我们发现细菌和酵母缺乏型突变体对IR不敏感，表明DNA链与末端3'阻断组而不是alphadn可能有助于细胞存活。我们提出了NFO和APN1的新型衬底特异性在抵消氧化DNA碱基损伤方面发挥着重要作用。

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