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Abstract：
Cellular stress response mechanisms typically increase organellar quantity and volume. To restore cellular homeostasis and organellar integrity, the surplus organelles are cleared by macroautophagy/autophagy, an intracellular process that shuttles cytoplasmic material to the lysosomes for degradation. The degradation is mediated by autophagy receptors that selectively link the degradable cargo to the autophagy machinery. Studies have identified receptors for the degradation of mitochondria, endoplasmic reticulum, lysosomes, and peroxisomes. The autophagic degradation of the Golgi, named Golgiphagy, however, has remained undefined. The Golgi is essential for the processing, sorting and trafficking of proteins and lipids in the secretory pathway. In a recent study, we identified CALCOCO1 as a Golgiphagy receptor in response to nutrient deprivation. CALCOCO1 interacts with Golgi membranes by binding to cytoplasmic Ankyrin repeat (AR) domains of Golgi resident ZDHHC17 and ZDHHC13 palmitoyltransferases (PATs) via a defined zDHHC-AR-binding motif (zDABM) to recruit autophagy machinery. Lack of CALCOCO1 in cells causes an impaired Golgiphagy and expansion of the Golgi.
摘要：
细胞应激反应机制通常会增加细胞器的数量和体积。为了恢复细胞稳态和细胞器完整性，多余的细胞器被巨自噬/自噬清除，将细胞质物质运送到溶酶体进行降解的细胞内过程。降解是由自噬受体介导的，自噬受体选择性地将可降解的货物与自噬机制联系起来。研究已经确定了线粒体降解的受体，内质网，溶酶体,和过氧化物酶体。高尔基体的自噬降解,叫Golgiphagy,然而,仍然未定义。高尔基对于加工至关重要，蛋白质和脂质在分泌途径中的分选和运输。在最近的一项研究中,我们将CALCOCO1鉴定为响应营养剥夺的Golgiphagy受体。CALCOCO1通过与高尔基常驻ZDHHC17和ZDHHC13棕榈酰转移酶（PAT）的细胞质锚蛋白重复（AR）结构域结合，通过确定的zDHHC-AR结合基序（zDABM）与高尔基膜相互作用，以募集自噬机制。细胞中缺乏CALCOCO1会导致高尔基体受损和扩张。
