做为一个重要的细胞器，线粒体与能量生产、自由基产生以及细胞死亡都密切相关。因此，线粒体的质量的监控对于细胞的功能维持十分重要，损伤的线粒体主要通过自噬的机制被清除掉。FUNDC1是我们鉴定的一个线粒体自噬受体，其通过和自噬关键蛋白LC3的相互作用调控缺氧等诱导的线粒体自噬。我们发现在线粒体自噬诱导的早期，FUNDC1会早于其他线粒体蛋白发生降解，而这种降解与线粒体定位的E3泛素酶MARCH5有关。我们计划研究MARCH5参与FUNDC1降解的具体分子机制，明确MARCH5在FUNDC1蛋白降解中的关键作用，进一步阐明在线粒体自噬诱导早期FUNDC1的降解对于线粒体功能维持的意义。我们的研究将有助于了解细胞通过调控线粒体自噬活性从而监控线粒体功能的具体机制。

Mitochondria are essential organelles for many fundamental cellular processes, including energy production, free radical generation and programmed cell death. It is therefore of pivotal importance to monitor the functional status of mitochondria and to remove damaged or unwanted mitochondrial by mitophagy FUNDC1 is a new mitophagy receptor which can interact with LC3 to mediate mitophagy in response to hypoxia. In an effort to understand the molecular regulation of FUNDC1 mediated mitophagy, we found that FUNDC1 became degraded prior to other mitochondrial proteins. Subsequently, we identified that MARCH5, a mitochondrial localized E3 ubiquitin ligase, is related to FUNDC1 ubiquitination and degradation. We will investigate the molecular mechanism of FUNDC1 degradation by MARCH5 and its biological significance for mitochondrial quality control. Our research will offer new understanding of how functional status of mitochondria is monitored to determined mitophagy activities.