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Wen Yang¹, Koji Nagasawa², Christian Münch¹

¹Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.

|November 25, 2016

概括

线粒体素 (SIRT3-5) 调节细胞压力. 我们发现SIRT3与ATP合成酶结合, 在压力下释放去乙蛋白并恢复线粒体功能.

科学领域:

线粒体生理学
细胞应激反应
酶调节

背景情况:

线粒体sirtuins (SIRT3-5) 是关键的NAD+依赖酶,参与应激适应.
了解它们的目标,调节和相互作用对于线粒体健康至关重要.
关键的挑战包括阐明sirtuin功能和监管机制的全部范围.

研究的目的:

使用系统蛋白质组学绘制线粒体蛋白相互作用网络.
确定新型的素基质和调节性相互作用.
揭示素相互作用在维护线粒体平衡中的作用.

主要方法:

系统性相互作用蛋白质组学以分析线粒体的 sirtuin 相互作用体.
生物化学测试和CRISPR/Cas9基因编辑以验证蛋白质相互作用和功能作用.
在体外复制实验以剖析分子机制.

主要成果:

发现SIRT3-5与线粒体功能模块的广泛相互作用.
确定了 mitochondrial sirtuins 的许多候选基质.
发现了一个关键的调节机制,其中SIRT3被ATP合成酶隔离.
在压力时,SIRT3从ATP合成酶中依赖于pH的释放,使蛋白质脱乙和膜潜能恢复.

结论:

线粒体的Sirtuin相互作用网络为未来的研究提供了一个全面的地图.
通过ATP合成酶封存SIRT3是线粒体平衡的一个关键调节机制.
在应激反应中,SIRT3通过依赖pH的调节其活性和基质相互作用发挥着至关重要的作用.

关键词:

酸合成酶乙化脱乙化能量稳态互动体膜潜力线粒体蛋白与蛋白的相互作用西尔图因它们的 pH

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