Chen Xi, Ballin Jeff D, Della-Maria Julie, Tsai Miaw-Sheue, White Elizabeth J, Tomkinson Alan E, Wilson Gerald M
Department of Radiation Oncology and Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
DNA Repair (Amst). 2009 Aug 6;8(8):961-8. doi: 10.1016/j.dnarep.2009.06.002. Epub 2009 Jul 8.
The three human LIG genes encode polypeptides that catalyze phosphodiester bond formation during DNA replication, recombination and repair. While numerous studies have identified protein partners of the human DNA ligases (hLigs), there has been little characterization of the catalytic properties of these enzymes. In this study, we developed and optimized a fluorescence-based DNA ligation assay to characterize the activities of purified hLigs. Although hLigI joins DNA nicks, it has no detectable activity on linear duplex DNA substrates with short, cohesive single-strand ends. By contrast, hLigIIIbeta and the hLigIIIalpha/XRCC1 and hLigIV/XRCC4 complexes are active on both nicked and linear duplex DNA substrates. Surprisingly, hLigIV/XRCC4, which is a key component of the major non-homologous end joining (NHEJ) pathway, is significantly less active than hLigIII on a linear duplex DNA substrate. Notably, hLigIV/XRCC4 molecules only catalyze a single ligation event in the absence or presence of ATP. The failure to catalyze subsequent ligation events reflects a defect in the enzyme-adenylation step of the next ligation reaction and suggests that, unless there is an in vivo mechanism to reactivate DNA ligase IV/XRCC4 following phosphodiester bond formation, the cellular NHEJ capacity will be determined by the number of adenylated DNA ligaseIV/XRCC4 molecules.
三种人类LIG基因编码的多肽在DNA复制、重组和修复过程中催化磷酸二酯键的形成。虽然众多研究已鉴定出人类DNA连接酶(hLigs)的蛋白质伴侣,但对这些酶的催化特性却鲜有描述。在本研究中,我们开发并优化了一种基于荧光的DNA连接测定法,以表征纯化的hLigs的活性。尽管hLigI可连接DNA切口,但它对具有短粘性单链末端的线性双链DNA底物没有可检测到的活性。相比之下,hLigIIIβ以及hLigIIIα/XRCC1和hLigIV/XRCC4复合物对切口和线性双链DNA底物均有活性。令人惊讶的是,作为主要非同源末端连接(NHEJ)途径关键组分的hLigIV/XRCC4,在直线双链DNA底物上的活性明显低于hLigIII。值得注意的是,无论有无ATP,hLigIV/XRCC4分子仅催化一次连接事件。无法催化后续连接事件反映出下一次连接反应的酶腺苷化步骤存在缺陷,这表明,除非存在一种体内机制在磷酸二酯键形成后重新激活DNA连接酶IV/XRCC4,否则细胞的NHEJ能力将由腺苷化的DNA连接酶IV/XRCC4分子数量决定。