Institut für Biochemie und Molekularbiologie, ZBMZ, Universität Freiburg, D-79104 Freiburg, Germany.
J Mol Biol. 2012 Nov 9;423(5):677-86. doi: 10.1016/j.jmb.2012.09.001. Epub 2012 Sep 10.
The mitochondrial inner membrane contains two non-bilayer-forming phospholipids, phosphatidylethanolamine (PE) and cardiolipin (CL). Lack of CL leads to destabilization of respiratory chain supercomplexes, a reduced activity of cytochrome c oxidase, and a reduced inner membrane potential Δψ. Although PE is more abundant than CL in the mitochondrial inner membrane, its role in biogenesis and assembly of inner membrane complexes is unknown. We report that similar to the lack of CL, PE depletion resulted in a decrease of Δψ and thus in an impaired import of preproteins into and across the inner membrane. The respiratory capacity and in particular the activity of cytochrome c oxidase were impaired in PE-depleted mitochondria, leading to the decrease of Δψ. In contrast to depletion of CL, depletion of PE did not destabilize respiratory chain supercomplexes but favored the formation of larger supercomplexes (megacomplexes) between the cytochrome bc(1) complex and the cytochrome c oxidase. We conclude that both PE and CL are required for a full activity of the mitochondrial respiratory chain and the efficient generation of the inner membrane potential. The mechanisms, however, are different since these non-bilayer-forming phospholipids exert opposite effects on the stability of respiratory chain supercomplexes.
线粒体的内膜含有两种非双层形成的磷脂，磷脂酰乙醇胺（PE）和心磷脂（CL）。缺乏 CL 会导致呼吸链超级复合物的不稳定，细胞色素 c 氧化酶的活性降低，以及内膜电位 Δψ 的降低。尽管 PE 在线粒体的内膜中比 CL 更丰富，但它在生物发生和内膜复合物的组装中的作用尚不清楚。我们报告说，与缺乏 CL 相似，PE 耗竭导致 Δψ 的降低，从而导致前蛋白向内膜的输入和跨膜受到损害。PE 耗竭的线粒体的呼吸能力，特别是细胞色素 c 氧化酶的活性受损，导致 Δψ 的降低。与 CL 的耗竭相反，PE 的耗竭并没有使呼吸链超级复合物不稳定，而是有利于细胞色素 bc（1）复合物和细胞色素 c 氧化酶之间形成更大的超级复合物（巨型复合物）。我们得出的结论是，PE 和 CL 都需要线粒体呼吸链的充分活性和有效产生内膜电位。然而，这些非双层形成的磷脂对呼吸链超级复合物的稳定性产生相反的影响，因此机制是不同的。
