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首页> 外文期刊>Molecular and Cellular Biology >Dynamic Compartmentalization of Base Excision Repair Proteins in Response to Nuclear and Mitochondrial Oxidative Stress
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Dynamic Compartmentalization of Base Excision Repair Proteins in Response to Nuclear and Mitochondrial Oxidative Stress

机译：碱基切除修复蛋白对核和线粒体氧化应激反应的动态区划。

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DNAs harbored in both nuclei and mitochondria of eukaryotic cells are subject to continuous oxidative damage resulting from normal metabolic activities or environmental insults. Oxidative DNA damage is primarily reversed by the base excision repair (BER) pathway, initiated by N-glycosylase apurinic/apyrimidinic (AP) lyase proteins. To execute an appropriate repair response, BER components must be distributed to accommodate levels of genotoxic stress that may vary considerably between nuclei and mitochondria, depending on the growth state and stress environment of the cell. Numerous examples exist where cells respond to signals, resulting in relocalization of proteins involved in key biological transactions. To address whether such dynamic localization contributes to efficient organelle-specific DNA repair, we determined the intracellular localization of the Saccharomyces cerevisiae N-glycosylase/AP lyases, Ntg1 and Ntg2, in response to nuclear and mitochondrial oxidative stress. Fluorescence microscopy revealed that Ntg1 is differentially localized to nuclei and mitochondria, likely in response to the oxidative DNA damage status of the organelle. Sumoylation is associated with targeting of Ntg1 to nuclei containing oxidative DNA damage. These studies demonstrate that trafficking of DNA repair proteins to organelles containing high levels of oxidative DNA damage may be a central point for regulating BER in response to oxidative stress.
机译：真核细胞的核和线粒体中都含有的DNA会由于正常的代谢活动或环境侵害而遭受持续的氧化损伤。氧化性DNA损伤主要通过碱基切除修复（BER）途径逆转，该途径由 N 糖基化酶嘌呤/嘧啶（AP）裂解酶蛋白引发。为了执行适当的修复反应，必须分配BER成分以适应遗传毒性应力的水平，该毒性水平可能在细胞核和线粒体之间变化，具体取决于细胞的生长状态和应力环境。存在许多例子，其中细胞响应信号，从而导致参与关键生物交易的蛋白质发生重新定位。为了解决这种动态定位是否有助于有效的细胞器特异性DNA修复，我们确定了啤酒酵母N 糖基化酶/ AP裂解酶Ntg1和Ntg2在细胞内的定位，以响应核和线粒体的氧化应激。荧光显微镜显示，Ntg1差异定位于细胞核和线粒体，可能是由于细胞器的氧化DNA损伤状态所致。 Sumoylation与Ntg1靶向含有氧化DNA损伤的细胞核相关。这些研究表明，DNA修复蛋白向含有高水平氧化DNA损伤的细胞器的运输可能是调节BER以响应氧化应激的中心点。

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