Mitochondrial membrane dynamics is a cellular rheostat that relates metabolic function and organelle morphology. Using an in vitro reconstitution system, we describe a mechanism for how mitochondrial inner-membrane fusion is regulated by the ratio of two forms of Opa1. We found that the long-form of Opa1 (l-Opa1) is sufficient for membrane docking, hemifusion and low levels of content release. However, stoichiometric levels of the processed, short form of Opa1 (s-Opa1) work together with l-Opa1 to mediate efficient and fast membrane pore opening. Additionally, we found that excess levels of s-Opa1 inhibit fusion activity, as seen under conditions of altered proteostasis. These observations describe a mechanism for gating membrane fusion.

中文翻译：

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两种形式的Opa1协同完成线粒体内膜的融合

线粒体膜动力学是与代谢功能和细胞器形态相关的细胞变阻器。使用体外重建系统，我们描述了两种形式的Opa1的比例如何调节线粒体内膜融合的机制。我们发现，Opa1（l-Opa1）的长形式足以用于膜对接，半融合和低含量的内容物释放。但是，化学计量水平的经处理的短形式的Opa1（s-Opa1）与l-Opa1共同起作用，可以介导有效且快速的膜孔打开。此外，我们发现过量的s-Opa1会抑制融合活性，如在蛋白稳态改变的条件下所见。这些观察结果描述了门控膜融合的机制。