Department of Biochemistry, University of California, Riverside, California 92521, United States.
Biochemistry. 2011 Jan 11;50(1):63-81. doi: 10.1021/bi1015937. Epub 2010 Dec 8.
In the current X-ray crystallographic structural models of photosystem II, Glu354 of the CP43 polypeptide is the only amino acid ligand of the oxygen-evolving Mn(4)Ca cluster that is not provided by the D1 polypeptide. To further explore the influence of this structurally unique residue on the properties of the Mn(4)Ca cluster, the CP43-E354Q mutant of the cyanobacterium Synechocystis sp. PCC 6803 was characterized with a variety of biophysical and spectroscopic methods, including polarography, EPR, X-ray absorption, FTIR, and mass spectrometry. The kinetics of oxygen release in the mutant were essentially unchanged from those in wild type. In addition, the oxygen flash yields exhibited normal period four oscillations having normal S state parameters, although the yields were lower, correlating with the mutant's lower steady-state rate (approximately 20% compared to wild type). Experiments conducted with H(2)(18)O showed that the fast and slow phases of substrate water exchange in CP43-E354Q thylakoid membranes were accelerated 8.5- and 1.8-fold, respectively, in the S(3) state compared to wild type. Purified oxygen-evolving CP43-E354Q PSII core complexes exhibited a slightly altered S(1) state Mn-EXAFS spectrum, a slightly altered S(2) state multiline EPR signal, a substantially altered S(2)-minus-S(1) FTIR difference spectrum, and an unusually long lifetime for the S(2) state (>10 h) in a substantial fraction of reaction centers. In contrast, the S(2) state Mn-EXAFS spectrum was nearly indistinguishable from that of wild type. The S(2)-minus-S(1) FTIR difference spectrum showed alterations throughout the amide and carboxylate stretching regions. Global labeling with (15)N and specific labeling with l-[1-(13)C]alanine revealed that the mutation perturbs both amide II and carboxylate stretching modes and shifts the symmetric carboxylate stretching modes of the α-COO(-) group of D1-Ala344 (the C-terminus of the D1 polypeptide) to higher frequencies by 3-4 cm(-1) in both the S(1) and S(2) states. The EPR and FTIR data implied that 76-82% of CP43-E354Q PSII centers can achieve the S(2) state and that most of these can achieve the S(3) state, but no evidence for advancement beyond the S(3) state was observed in the FTIR data, at least not in a majority of PSII centers. Although the X-ray absorption and EPR data showed that the CP43-E354Q mutation only subtly perturbs the structure and spin state of the Mn(4)Ca cluster in the S(2) state, the FTIR and H(2)(18)O exchange data show that the mutation strongly influences other properties of the Mn(4)Ca cluster, altering the response of numerous carboxylate and amide groups to the increased positive charge that develops on the cluster during the S(1) to S(2) transition and weakening the binding of both substrate water molecules (or water-derived ligands), especially the one that exchanges rapidly in the S(3) state. The FTIR data provide evidence that CP43-Glu354 coordinates to the Mn(4)Ca cluster in the S(1) state as a bridging ligand between two metal ions but provide no compelling evidence that this residue changes its coordination mode during the S(1) to S(2) transition. The H(2)(18)O exchange data provide evidence that CP43-Glu354 interacts with the Mn ion that ligates the substrate water molecule (or water-derived ligand) that is in rapid exchange in the S(3) state.
在当前光合作用系统 II 的 X 射线晶体结构模型中,CP43 多肽中的 Glu354 是唯一不是由 D1 多肽提供的氧释放 Mn(4)Ca 簇的氨基酸配体。为了进一步探讨这个结构独特的残基对 Mn(4)Ca 簇性质的影响,对蓝细菌集胞藻 6803 的 CP43-E354Q 突变体进行了各种生物物理和光谱方法的研究,包括极谱法、EPR、X 射线吸收、FTIR 和质谱法。突变体中氧气释放的动力学与野生型基本相同。此外,虽然氧气闪光产率较低,与突变体的稳态速率(约为野生型的 20%)相关,但仍表现出正常的周期四振荡,具有正常的 S 态参数。在 H(2)(18)O 实验中表明,CP43-E354Q 类囊体膜中底物水交换的快相和慢相在 S(3)态下分别比野生型加速了 8.5 倍和 1.8 倍。纯化的产氧 CP43-E354Q PSII 核心复合物表现出轻微改变的 S(1)态 Mn-EXAFS 光谱、轻微改变的 S(2)态多线 EPR 信号、显著改变的 S(2)-minus-S(1)FTIR 差谱,以及相当一部分反应中心中 S(2)态的异常长寿命(>10 h)。相比之下,S(2)态 Mn-EXAFS 光谱与野生型几乎无法区分。S(2)-minus-S(1)FTIR 差谱显示酰胺和羧酸盐伸缩区域的变化。用(15)N 进行全局标记和用 l-[1-(13)C]丙氨酸进行特异性标记表明,该突变扰乱了酰胺 II 和羧酸盐伸缩模式,并使 D1-Ala344(D1 多肽的 C 末端)的α-COO(-)基团的对称羧酸盐伸缩模式在 S(1)和 S(2)态下向更高的频率移动了 3-4 cm(-1)。EPR 和 FTIR 数据表明,76-82%的 CP43-E354Q PSII 中心可以达到 S(2)态,并且大多数中心可以达到 S(3)态,但在 FTIR 数据中没有观察到超过 S(3)态的证据,至少在大多数 PSII 中心中没有。虽然 X 射线吸收和 EPR 数据表明 CP43-E354Q 突变仅轻微扰乱了 S(2)态 Mn(4)Ca 簇的结构和自旋态,但 FTIR 和 H(2)(18)O 交换数据表明,该突变强烈影响了 Mn(4)Ca 簇的其他性质,改变了许多羧酸盐和酰胺基团对 S(1)到 S(2)转变过程中簇上增加的正电荷的响应,并削弱了底物水分子(或衍生的水分子)的结合,特别是在 S(3)态下快速交换的水分子。FTIR 数据提供了证据,表明 CP43-Glu354 在 S(1)态作为两个金属离子之间的桥联配体与 Mn(4)Ca 簇配位,但没有令人信服的证据表明该残基在 S(1)到 S(2)转变过程中改变了其配位模式。H(2)(18)O 交换数据提供了证据,表明 CP43-Glu354 与 Mn 离子相互作用,Mn 离子与 S(3)态中快速交换的底物水分子(或衍生的水分子)配位。