Kuo C F, McRee D E, Fisher C L, O'Handley S F, Cunningham R P, Tainer J A
Department of Molecular Biology, Scripps Research Institute, La Jolla, CA 92037.
Science. 1992 Oct 16;258(5081):434-40. doi: 10.1126/science.1411536.
The crystal structure of the DNA repair enzyme endonuclease III, which recognizes and cleaves DNA at damaged bases, has been solved to 2.0 angstrom resolution with an R factor of 0.185. This iron-sulfur [4Fe-4S] enzyme is elongated and bilobal with a deep cleft separating two similarly sized domains: a novel, sequence-continuous, six-helix domain (residues 22 to 132) and a Greek-key, four-helix domain formed by the amino-terminal and three carboxyl-terminal helices (residues 1 to 21 and 133 to 211) together with the [4Fe-4S] cluster. The cluster is bound entirely within the carboxyl-terminal loop with a ligation pattern (Cys-X6-Cys-X2-Cys-X5-Cys) distinct from all other known [4Fe-4S] proteins. Sequence conservation and the positive electrostatic potential of conserved regions identify a surface suitable for binding duplex B-DNA across the long axis of the enzyme, matching a 46 angstrom length of protected DNA. The primary role of the [4Fe-4S] cluster appears to involve positioning conserved basic residues for interaction with the DNA phosphate backbone. The crystallographically identified inhibitor binding region, which recognizes the damaged base thymine glycol, is a seven-residue beta-hairpin (residues 113 to 119). Location and side chain orientation at the base of the inhibitor binding site implicate Glu112 in the N-glycosylase mechanism and Lys120 in the beta-elimination mechanism. Overall, the structure reveals an unusual fold and a new biological function for [4Fe-4S] clusters and provides a structural basis for studying recognition of damaged DNA and the N-glycosylase and apurinic/apyrimidinic-lyase mechanisms.
DNA修复酶核酸内切酶III可识别受损碱基并在该处切割DNA,其晶体结构已解析到2.0埃的分辨率,R因子为0.185。这种铁硫[4Fe-4S]酶呈细长的双叶状,有一个深裂缝将两个大小相似的结构域分开:一个新的、序列连续的六螺旋结构域(第22至132位氨基酸残基)和一个由氨基末端螺旋和三个羧基末端螺旋形成的希腊钥匙型四螺旋结构域(第1至21位氨基酸残基和第133至211位氨基酸残基)以及[4Fe-4S]簇。该簇完全结合在羧基末端环内,其连接模式(半胱氨酸-X6-半胱氨酸-X2-半胱氨酸-X5-半胱氨酸)与所有其他已知的[4Fe-4S]蛋白不同。序列保守性和保守区域的正静电势确定了一个适合在酶的长轴上结合双链B-DNA的表面,与46埃长的受保护DNA相匹配。[4Fe-4S]簇的主要作用似乎是定位保守的碱性残基以与DNA磷酸骨架相互作用。晶体学鉴定的抑制剂结合区域可识别受损碱基胸腺嘧啶二醇,是一个七残基的β-发夹结构(第113至119位氨基酸残基)。抑制剂结合位点底部的位置和侧链方向表明,谷氨酸112参与N-糖基化酶机制,赖氨酸120参与β-消除机制。总体而言,该结构揭示了[4Fe-4S]簇的一种不寻常折叠和新的生物学功能,并为研究受损DNA的识别以及N-糖基化酶和脱嘌呤/脱嘧啶裂合酶机制提供了结构基础。