Nam Gyu Hyun, Cha Sun-Shin, Yun Young Sung, Oh Yun Hee, Hong Bee Hak, Lee Heung-Soo, Choi Kwan Yong
National Research Laboratory of Protein Folding and Engineering, Pohang 790-784, Republic of Korea.
Biochem J. 2003 Oct 15;375(Pt 2):297-305. doi: 10.1042/BJ20030263.
KSI (ketosteroid isomerase) from Comamonas testosteroni is a homodimeric enzyme that catalyses the allylic isomerization of Delta5-3-ketosteroids to their conjugated Delta4-isomers at a reaction rate equivalent to the diffusion-controlled limit. Based on the structural analysis of KSI at a high resolution, the conserved cis-Pro39 residue was proposed to be involved in the proper positioning of Asp38, a critical catalytic residue, since the residue was found not only to be structurally associated with Asp38, but also to confer a structural rigidity on the local active-site geometry consisting of Asp38, Pro39, Val40, Gly41 and Ser42 at the flexible loop between b-strands B1 and B2. In order to investigate the structural role of the conserved cis-Pro39 residue near the active site of KSI, Pro39 was replaced with alanine or glycine. The free energy of activation for the P39A and P39G mutants increased by 10.5 and 16.7 kJ/mol (2.5 and 4.0 kcal/mol) respectively, while DG(U)H2O (the free-energy change for unfolding in the absence of urea at 25.00+/-0.02 degrees C) decreased by 31.0 and 35.6 kJ/mol (7.4 and 8.5 kcal/mol) respectively, compared with the wild-type enzyme. The crystal structure of the P39A mutant in complex with d-equilenin [d-1,3,5(10),6,8-estrapentaen-3-ol-17-one], a reaction intermediate analogue, determined at 2.3 A (0.23 nm) resolution revealed that the P39A mutation significantly disrupted the proper orientations of both d-equilenin and Asp38, as well as the local active-site geometry near Asp38, which resulted in substantial decreases in the activity and stability of KSI. Upon binding 1-anilinonaphthalene-8-sulphonic acid, the fluorescence intensities of the P39A and P39G mutants were increased drastically, with maximum wavelengths blue-shifted upon binding, indicating that the mutations might alter the hydrophobic active site of KSI. Taken together, our results demonstrate that the conserved cis-Pro39 residue plays a crucial role in the proper positioning of the critical catalytic base Asp38 and in the structural integrity of the active site in KSI.
睾丸酮丛毛单胞菌的KSI(酮甾体异构酶)是一种同二聚体酶,它能以相当于扩散控制极限的反应速率催化Δ5-3-酮甾体向其共轭Δ4-异构体的烯丙基异构化反应。基于对KSI的高分辨率结构分析,保守的顺式Pro39残基被认为参与关键催化残基Asp38的正确定位,因为该残基不仅在结构上与Asp38相关联,而且赋予由β链B1和B2之间的柔性环上的Asp38、Pro39、Val40、Gly41和Ser42组成的局部活性位点几何结构以结构刚性。为了研究KSI活性位点附近保守的顺式Pro39残基的结构作用,将Pro39替换为丙氨酸或甘氨酸。P39A和P39G突变体的活化自由能分别增加了10.5和16.7 kJ/mol(2.5和4.0 kcal/mol),而与野生型酶相比,DG(U)H2O(在25.00±0.02℃无尿素时展开的自由能变化)分别降低了31.0和35.6 kJ/mol(7.4和8.5 kcal/mol)。以2.3 Å(0.23 nm)分辨率测定的与反应中间体类似物d-马萘雌酮[d-1,3,5(10),6,8-雌甾五烯-3-醇-17-酮]复合的P39A突变体的晶体结构表明,P39A突变显著破坏了d-马萘雌酮和Asp38的正确取向以及Asp38附近的局部活性位点几何结构,这导致KSI的活性和稳定性大幅下降。在结合1-苯胺基萘-8-磺酸后,P39A和P39G突变体的荧光强度急剧增加,结合后最大波长发生蓝移,表明这些突变可能改变了KSI的疏水活性位点。综上所述,我们的结果表明,保守的顺式Pro39残基在关键催化碱基Asp38的正确定位以及KSI活性位点的结构完整性中起着至关重要的作用。