CALCOCO1, also known as calcium binding and coiled-coil domain 1, is an important autophagy receptor. It is involved in reticulophagy and golgiphagy, which are key processes in maintaining cellular homeostasis by selectively degrading the endoplasmic reticulum (ER) and Golgi apparatus respectively. These pathways are crucial for cells to respond to stress stimuli such as nutrient deprivation, misfolded protein accumulation, etc. Genetic models, like gene knockout models, are valuable for studying CALCOCO1's function [1-10].

Depletion of CALCOCO1 in cultured cells leads to impaired ER degradation during stress, as it acts as a soluble reticulophagy receptor for the degradation of tubular ER. It binds to VAPA and VAPB on the ER membrane via a FFAT-like motif and recruits autophagy machinery through LIR and UIR motifs [2,3]. In the context of Golgi, lack of CALCOCO1 in cells causes impaired golgiphagy and Golgi expansion. CALCOCO1 binds to Golgi-resident ZDHHC17 and ZDHHC13 palmitoyltransferases via a zDABM motif to recruit autophagy machinery for Golgi degradation [1,4].

In conclusion, CALCOCO1 plays essential roles in maintaining cellular homeostasis through its functions in reticulophagy and golgiphagy. Model-based research, especially through CALCOCO1-deficient models, has revealed its significance in processes related to ER and Golgi homeostasis. Although no specific disease areas directly related to CALCOCO1 KO/CKO mouse models are given in the provided references, understanding its functions may potentially contribute to studying diseases associated with disrupted autophagy of the ER and Golgi in the future [1-10].