Atg14-KO Mouse

Atg14, also known as autophagy-related 14, is a key regulator in the autophagy process. It is an essential component for the fusion of autophagosomes with lysosomes, which is crucial for the degradation of autophagic cargo. Autophagy is a cellular pathway involved in maintaining cellular homeostasis, and Atg14's role in this pathway is of great biological importance. Genetic models, such as gene knockout mouse models, have been valuable in studying its function [1,2,3].

In macrophages, reduction of Atg14 expression leads to impaired autophagy function, and overexpression of Atg14 by adenovirus enhances autophagosome-lysosome fusion, promotes lipid degradation, decreases apoptosis and inflammatory response, and alleviates atherosclerotic lesions in apoe-/-mice [1]. In hepatocytes, Atg14 is enriched on lipid droplets. Its deficiency decreases triglyceride hydrolysis, suggesting it plays a critical role in hepatic lipid droplet homeostasis [2]. Additionally, coronavirus hijacks the STX18-Atg14 axis-regulated lipophagy to evade an anti-viral effect, as knockdown of STX18 induces degradation of an anti-viral protein dependent on Atg14-mediated lipophagy [3].

In conclusion, Atg14 is essential for autophagy-related processes such as autophagosome-lysosome fusion and lipophagy. Studies using gene knockout models have revealed its significant roles in diseases like atherosclerosis and in viral-host interactions. Understanding Atg14's functions provides insights into the mechanisms of these biological processes and disease conditions, potentially offering new therapeutic targets.