Ahmad Zulfiqar, Winjobi Mumeenat, Kabir M Anaul
Department of Biochemistry, Kirksville College of Osteopathic Medicine, A. T. Still University of Health Sciences , Kirksville, Missouri 63501, United States.
Biochemistry. 2014 Dec 2;53(47):7376-85. doi: 10.1021/bi5013063. Epub 2014 Nov 17.
This paper describes the role of α-subunit VISIT-DG sequence residue αThr-349 in the catalytic sites of Escherichia coli F1Fo ATP synthase. X-ray structures show the highly conserved αThr-349 in the proximity (2.68 Å) of the conserved phosphate binding residue βR182 in the phosphate binding subdomain. αT349A, -D, -Q, and -R mutations caused 90-100-fold losses of oxidative phosphorylation and reduced ATPase activity of F1Fo in membranes. Double mutation αT349R/βR182A was able to partially compensate for the absence of known phosphate binding residue βR182. Azide, fluoroaluminate, and fluoroscandium caused insignificant inhibition of αT349A, -D, and -Q mutants, slight inhibition of the αT349R mutant, partial inhibition of the αT349R/βR182A double mutant, and complete inhibition of the wild type. Whereas NBD-Cl (7-chloro-4-nitrobenzo-2-oxa-1,3-diazole) inhibited wild-type ATPase and its αT349A, -D, -R, and -Q mutants essentially completely, βR182A ATPase and double mutant αT349A/βR182A were inhibited partially. Inhibition characteristics supported the conclusion that NBD-Cl reacts in βE (empty) catalytic sites, as shown previously by X-ray structure analysis. Phosphate protected against NBD-Cl inhibition in the wild type, αT349R, and double mutant αT349R/βR182A but not in αT349A, αT349D, or αT349Q. The results demonstrate that αThr-349 is a supplementary residue involved in phosphate binding and transition state stabilization in ATP synthase catalytic sites through its interaction with βR182.
本文描述了α亚基VISIT - DG序列残基αThr - 349在大肠杆菌F1Fo ATP合酶催化位点中的作用。X射线结构显示,高度保守的αThr - 349位于磷酸结合亚结构域中保守的磷酸结合残基βR182附近(2.68 Å)。αT349A、- D、- Q和- R突变导致氧化磷酸化损失90 - 100倍,并降低了膜中F1Fo的ATP酶活性。双突变αT349R/βR182A能够部分补偿已知磷酸结合残基βR182的缺失。叠氮化物、氟铝酸盐和氟钪对αT349A、- D和- Q突变体的抑制作用不显著,对αT349R突变体有轻微抑制作用,对αT349R/βR182A双突变体有部分抑制作用,对野生型有完全抑制作用。而NBD - Cl(7 - 氯 - 4 - 硝基苯并 - 2 - 恶唑 - 1,3 - 二氮杂环戊二烯)基本上完全抑制野生型ATP酶及其αT349A、- D、- R和- Q突变体,对βR182A ATP酶和双突变体αT349A/βR182A有部分抑制作用。抑制特性支持了NBD - Cl在βE(空)催化位点发生反应的结论,如先前X射线结构分析所示。磷酸盐在野生型、αT349R和双突变体αT349R/βR182A中可防止NBD - Cl抑制,但在αT349A、αT349D或αT349Q中则不能。结果表明,αThr - 349是一个通过与βR182相互作用参与ATP合酶催化位点中磷酸结合和过渡态稳定的补充残基。