Fetter J R, Qian J, Shapleigh J, Thomas J W, García-Horsman A, Schmidt E, Hosler J, Babcock G T, Gennis R B, Ferguson-Miller S
Department of Biochemistry, Michigan State University, East Lansing 48824.
Proc Natl Acad Sci U S A. 1995 Feb 28;92(5):1604-8. doi: 10.1073/pnas.92.5.1604.
As the final electron acceptor in the respiratory chain of eukaryotic and many prokaryotic organisms, cytochrome c oxidase (EC 1.9.3.1) catalyzes the reduction of oxygen to water and generates a proton gradient. To test for proton pathways through the oxidase, site-directed mutagenesis was applied to subunit I of the Rhodobacter sphaeroides enzyme. Mutants were characterized in three highly conserved regions of the peptide, comprising possible proton loading, unloading, and transfer sites: an interior loop between helices II and III (Asp132Asn/Ala), an exterior loop between helices IX and X (His411Ala, Asp412Asn, Thr413Asn, Tyr414Phe), and the predicted transmembrane helix VIII (Thr352Ala, Pro358Ala, Thr359Ala, Lys362Met). Most of the mutants had lower activity than wild type, but only mutants at residue 132 lost proton pumping while retaining electron transfer activity. Although electron transfer was substantially inhibited, no major structural alteration appears to have occurred in D132 mutants, since resonance Raman and visible absorbance spectra were normal. However, lower CO binding (70-85% of wild type) suggests some minor change to the binuclear center. In addition, the activity of the reconstituted Asp132 mutants was inhibited rather than stimulated by ionophores or uncoupler. The inhibition was not observed with the purified enzyme and a direct pH effect was ruled out, suggesting an altered response to the electrical or pH gradient. The results support an important role for the conserved II-III loop in the proton pumping process and are consistent with the possibility of involvement of residues in helix VIII and the IX-X loop.
作为真核生物和许多原核生物呼吸链中的最终电子受体,细胞色素c氧化酶(EC 1.9.3.1)催化氧气还原为水并产生质子梯度。为了测试通过该氧化酶的质子途径,对球形红细菌酶的亚基I进行了定点诱变。对肽段的三个高度保守区域中的突变体进行了表征,这些区域包括可能的质子加载、卸载和转移位点:螺旋II和III之间的内部环(Asp132Asn/Ala)、螺旋IX和X之间的外部环(His411Ala、Asp412Asn、Thr413Asn、Tyr414Phe)以及预测的跨膜螺旋VIII(Thr352Ala、Pro358Ala、Thr359Ala、Lys362Met)。大多数突变体的活性低于野生型,但只有第132位残基处的突变体在保留电子转移活性的同时失去了质子泵浦功能。尽管电子转移受到了显著抑制,但D132突变体似乎没有发生重大结构改变,因为共振拉曼光谱和可见吸收光谱正常。然而,较低的CO结合能力(野生型的70 - 85%)表明双核中心有一些微小变化。此外,重组的Asp132突变体的活性受到离子载体或解偶联剂的抑制而非刺激。在纯化的酶中未观察到这种抑制作用,并且排除了直接的pH效应,这表明对电或pH梯度的反应发生了改变。结果支持了保守的II - III环在质子泵浦过程中的重要作用,并且与螺旋VIII和IX - X环中的残基参与其中的可能性一致。