Meiners Matthew J, Tahmaseb Kambiz, Matson Steven W
From the Department of Biology.
From the Department of Biology, Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599
J Biol Chem. 2014 Jun 13;289(24):17100-10. doi: 10.1074/jbc.M114.565309. Epub 2014 May 5.
DNA helicases use energy derived from nucleoside 5'-triphosphate hydrolysis to catalyze the separation of double-stranded DNA into single-stranded intermediates for replication, recombination, and repair. Escherichia coli helicase II (UvrD) functions in methyl-directed mismatch repair, nucleotide excision repair, and homologous recombination. A previously discovered 2-amino acid substitution of residues 403 and 404 (both Asp → Ala) in the 2B subdomain of UvrD (uvrD303) confers an antimutator and UV-sensitive phenotype on cells expressing this allele. The purified protein exhibits a "hyper-helicase" unwinding activity in vitro. Using rapid quench, pre-steady state kinetic experiments we show the increased helicase activity of UvrD303 is due to an increase in the processivity of the unwinding reaction. We suggest that this mutation in the 2B subdomain results in a weakened interaction with the 1B subdomain, allowing the helicase to adopt a more open conformation. This is consistent with the idea that the 2B subdomain may have an autoregulatory role. The UvrD303 mutation may enable the helicase to unwind DNA via a "strand displacement" mechanism, which is similar to the mechanism used to processively translocate along single-stranded DNA, and the increased unwinding processivity may contribute directly to the antimutator phenotype.
DNA解旋酶利用核苷5'-三磷酸水解产生的能量,催化双链DNA分离成单链中间体,用于复制、重组和修复。大肠杆菌解旋酶II(UvrD)在甲基导向错配修复、核苷酸切除修复和同源重组中发挥作用。先前发现的UvrD 2B亚结构域中第403和404位残基(均为天冬氨酸→丙氨酸)的2个氨基酸取代(uvrD303)赋予表达该等位基因的细胞抗突变和对紫外线敏感的表型。纯化后的蛋白在体外表现出“超解旋酶”解旋活性。通过快速淬灭、稳态前动力学实验,我们发现UvrD303解旋酶活性增加是由于解旋反应的持续合成能力增强。我们认为,2B亚结构域中的这种突变导致与1B亚结构域的相互作用减弱,使解旋酶能够采用更开放的构象。这与2B亚结构域可能具有自动调节作用的观点一致。UvrD303突变可能使解旋酶通过“链置换”机制解开DNA,这类似于用于沿单链DNA持续易位的机制,解旋持续合成能力的增加可能直接导致抗突变表型。