Atg7-flox Mouse

Atg7, an autophagy-related gene, is essential for classical degradative macroautophagy and cell cycle regulation. It acts as an E1-like activating enzyme, facilitating the conjugation of microtubule-associated protein light chain 3 (LC3)-phosphatidylethanolamine and ATG12, standing at the hub of ubiquitin-like systems in autophagic vesicle expansion. Atg7 is involved in multiple biological processes such as autophagy, adipogenesis, angiogenesis, and immune responses, and is crucial for maintaining cellular homeostasis and organismal health [1,2,4,5,6].

In adipose-selective fto knockout mice, FTO deficiency decreased white fat mass and impaired ATG7-dependent autophagy, indicating that m6A methylation machinery regulates autophagy and adipogenesis through targeting Atg7 [1]. Endothelial cell-specific Atg7 knockout (atg7 KO) mice showed impaired angiogenesis, delayed blood flow reperfusion, and reduced HIF1A expression due to up-regulation of STAT1 [2]. In Atg7-ECKO mice, there was astrocyte-microvascular disassociation, BBB leakage, and down-regulation of fibronectin, suggesting Atg7 is required for maintaining BBB homeostasis [3].

In conclusion, Atg7 is central to autophagy and has diverse functions in multiple biological processes. Gene knockout models, especially KO and CKO mouse models, have revealed its roles in adipogenesis, angiogenesis, and blood-brain barrier maintenance. Understanding Atg7 provides insights into the mechanisms of related diseases, potentially leading to new therapeutic strategies for obesity, cancer, and cardiovascular diseases [1,2,3].