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首页> 外文期刊>Biochemistry >Contributions of an endonuclease IV homologue to DNA repair in the African swine fever virus
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Contributions of an endonuclease IV homologue to DNA repair in the African swine fever virus

机译：核酸内切酶IV同源物对非洲猪瘟病毒DNA修复的贡献

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We recently demonstrated that African swine fever virus DNA polymerase X (Pol X) is extremely error-prone during single-nucleotide gap-filling and that the downstream ASFV DNA ligase seals 3' mismatched nicks with high efficiency. To further assess the credence of our hypothesis that these proteins may promote viral diversification by functioning within the context of an aberrant DNA repair pathway, herein we characterize the third protein expected to function in this system, a putative AP endonuclease (APE). Assays of the purified protein using oligonucleotide substrates unequivocally establish canonical APE activity, 3'-phosphatase and 3'-phosphodiesterase activities (in the context of a single-nucleotide gap), 3' -> 5' exonuclease activity (in the context of a nick), and nucleotide incision repair activity against 5,6-dihydrothymine. The 3' -> 5' exonuclease activity is shown to be highly dependent upon the identity of the nascent 3' base pair and to be inhibited when 2-deoxyribose-5-phosphate, rather than phosphate, constitutes the 5' moiety of the nick. ASFV APE retains activity when assayed in the presence of EDTA but is inactivated by incubation with 1,10-phenanthroline in the absence of a substrate, suggesting that it is an endonuclease IV homologue possessing intrinsic metal cofactors. The activities of ASFV APE, when considered alongside those of Pol X and ASFV DNA ligase, provide an enhanced understanding of (i) the types of damage that are likely to be sustained by the viral genome and (ii) the mechanisms by which the minimalist ASFV DNA repair pathway, consisting of just these three proteins, contributes to the fitness of the virus.
机译：我们最近证明，非洲猪瘟病毒DNA聚合酶X（Pol X）在单核苷酸缺口填充过程中极易出错，而下游ASFV DNA连接酶可高效密封3'不匹配的缺口。为了进一步评估我们的假设的可信度，即这些蛋白质可通过在异常DNA修复途径的背景下发挥功能来促进病毒多样化，在此我们表征了预期在该系统中发挥功能的第三个蛋白质，即假定的AP核酸内切酶（APE）。使用寡核苷酸底物对纯化的蛋白质进行的分析明确确定了规范的APE活性，3'-磷酸酶和3'-磷酸二酯酶活性（在单核苷酸缺口的情况下），3'-> 5'核酸外切酶活性（在切口），以及针对5,6-二氢胸腺嘧啶的核苷酸切口修复活性。已显示3'-> 5'核酸外切酶活性高度依赖于新生的3'碱基对的身份，并且当2-脱氧核糖-5-磷酸而不是磷酸构成缺口的5'部分时，其被抑制。当在EDTA存在下测定时，ASFV APE保留活性，但在不存在底物的情况下与1,10-菲咯啉一起孵育可使其失活，这表明它是具有内在金属辅因子的核酸内切酶IV同源物。当将ASFV APE的活性与Pol X和ASFV DNA连接酶的活性一起考虑时，可以更好地理解（i）病毒基因组可能遭受的损害类型以及（ii）极简主义者的机制仅由这三种蛋白质组成的ASFV DNA修复途径有助于病毒的适应性。

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