细胞自噬是细胞自我降解的一个细胞过程。在这个过程中，细胞将诸如线粒体之类的细胞器以及需要降解的胞浆物质包裹并运送至溶酶体降解。降解产生的氨基酸和其他一些小分子物质可被再利用或产生能量。根据底物种类、转运方式和调控机制的不同，细胞自噬可分为巨自噬，微自噬以及分子伴侣介导的自噬。细胞自噬是细胞应对“饥饿”和病原的一种重要手段，同时也是细胞清除受损细胞器以及其他有害物质的重要机制。细胞自噬异常会诱发诸如老年痴呆、帕金森等神经退行性疾病。细胞自噬的分子机制和所需蛋白在真核生物的各个物种中十分保守。其中参与细胞自噬起始的膜蛋白Atg9已被证明与帕金森病有密切关系。目前，Atg9定位异常诱发帕金森病的分子机制尚不清楚。因此，对Atg9结构和功能的研究不仅能够加深我们对细胞自噬起始分子机制的认知，还将帮助我们理解细胞自噬异常引起的帕金森病的分子机制。

Macroautophagy denotes a class of bulk and selective cellular self-consumptive processes that delivery mitochondria and the cytoplasmic component to lysosome for degradation. These processes are classified according to their substrates as starvation-induced bulk autophagy, the destruction of damaged mitochondria by mitophagy, sequestration of cytosolic pathogens by xenophagy, and many others. Not only does autophagy play an important role in response to starvation and phathogens, but also is an indispensable way of getting rid of damaged organelles and harmful stuff in cells. Many neurodegenerative diseases, e.g. Alzheimer's disease, Parkinson's diseases, are related to the abnormal autophagy. The core autophagy machineries are conserved across species. Among them, Atg9, which is indispensable to the initiation of autophagy, is related to Parkinson's disease. Up to date, the molecular mechanism of which the mislocation of Atg9 induces Parkinson's disease is yet elusive. Therefore, the structural and functional study of Atg9 will rich our knowledge of autophagy, as well as shed light on the mechanism of how abnormal autophagy causes Parkinson's disease