Department of Biochemistry, Emory University School of Medicine, Atlanta, Georgia, USA.
Prog Mol Biol Transl Sci. 2012;110:93-121. doi: 10.1016/B978-0-12-387665-2.00005-5.
This chapter discusses base excision repair (BER) and the known mechanisms defined thus far regulating BER in eukaryotes. Unlike the situation with nucleotide excision repair and double-strand break repair, little is known about how BER is regulated to allow for efficient and accurate repair of many types of DNA base damage in both nuclear and mitochondrial genomes. Regulation of BER has been proposed to occur at multiple, different levels including transcription, posttranslational modification, protein-protein interactions, and protein localization; however, none of these regulatory mechanisms characterized thus far affect a large spectrum of BER proteins. This chapter discusses a recently discovered mode of BER regulation defined in budding yeast cells that involves mobilization of DNA repair proteins to DNA-containing organelles in response to genotoxic stress.
本章讨论碱基切除修复(BER)以及目前已知的调节真核生物 BER 的机制。与核苷酸切除修复和双链断裂修复的情况不同,对于 BER 如何调节以允许在核和线粒体基因组中有效和准确地修复多种类型的 DNA 碱基损伤知之甚少。BER 的调节被提议发生在多个不同的水平,包括转录、翻译后修饰、蛋白质-蛋白质相互作用和蛋白质定位;然而,迄今为止,这些调节机制都没有影响到大量的 BER 蛋白。本章讨论了一种新发现的 BER 调节模式,该模式在芽殖酵母细胞中定义,涉及到在遗传毒性应激下,DNA 修复蛋白向含有 DNA 的细胞器的动员。