Division of Medical Genetics and Genomics, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou 310052, China.
Institute of Genetics, Department of Genetics, Zhejiang University School of Medicine, Hangzhou 310058, China.
Int J Mol Sci. 2022 Sep 17;23(18):10877. doi: 10.3390/ijms231810877.
The ADP/ATP carrier (AAC) plays a central role in oxidative metabolism by exchanging ATP and ADP across the inner mitochondrial membrane. Previous experiments have shown the involvement of the matrix loops of AAC in its function, yet potential mechanisms remain largely elusive. One obstacle is the limited information on the structural dynamics of the matrix loops. In the current work, unbiased all-atom molecular dynamics (MD) simulations were carried out on c-state wild-type AAC and mutants. Our results reveal that: (1) two ends of a matrix loop are tethered through interactions between the residue of triplet 38 (Q38, D143 and Q240) located at the C-end of the odd-numbered helix and residues of the [YF]xG motif located before the N-end of the short matrix helix in the same domain; (2) the initial progression direction of a matrix loop is determined by interactions between the negatively charged residue of the [DE]G motif located at the C-end of the short matrix helix and the capping arginine (R30, R139 and R236) in the previous domain; (3) the two chemically similar residues D and E in the highly conserved [DE]G motif are actually quite different; (4) the N-end of the M3 loop is clamped by the [DE]G motif and the capping arginine of domain 2 from the two sides, which strengthens interactions between domain 2 and domain 3; and (5) a highly asymmetric stable core exists within domains 2 and 3 at the m-gate level. Moreover, our results help explain almost all extremely conserved residues within the matrix loops of the ADP/ATP carriers from a structural point of view. Taken together, the current work highlights asymmetry in the three matrix loops and implies a close relationship between asymmetry and ADP/ATP transport.
ADP/ATP 载体 (AAC) 通过在内膜上交换 ATP 和 ADP 来发挥其在氧化代谢中的核心作用。先前的实验表明 AAC 的基质环参与了其功能,但潜在的机制在很大程度上仍难以捉摸。一个障碍是基质环结构动力学的信息有限。在目前的工作中,对 c 态野生型 AAC 和突变体进行了无偏的全原子分子动力学 (MD) 模拟。我们的结果表明:(1)基质环的两端通过位于奇数号螺旋 C 端的三联体 38 残基 (Q38、D143 和 Q240) 与位于短基质螺旋 N 端之前的 [YF]xG 基序中的残基之间的相互作用而被束缚在一起;(2)基质环的初始前进方向由位于短基质螺旋 C 端的 [DE]G 基序中带负电荷的残基与前一个域中的封端精氨酸 (R30、R139 和 R236) 之间的相互作用决定;(3)[DE]G 基序中高度保守的两个化学相似的残基 D 和 E 实际上非常不同;(4)M3 环的 N 端被 [DE]G 基序和来自 2 域的封端精氨酸从两侧夹住,从而增强了 2 域和 3 域之间的相互作用;(5)m 门水平上,2 域和 3 域内存在高度不对称的稳定核心。此外,我们的结果从结构角度帮助解释了 ADP/ATP 载体的基质环中几乎所有高度保守的残基。总的来说,目前的工作强调了三个基质环的不对称性,并暗示了不对称性与 ADP/ATP 转运之间的密切关系。