Gcn1 is a highly conserved protein present across eukaryotes. It is an essential effector for the kinase Gcn2, playing a pivotal role in integrated stress responses like amino acid starvation and oxidative stress. By interacting with Gcn2, it activates downstream signaling cascades. Additionally, Gcn1 acts as a ribosome collision sensor, contributing to the translation quality control pathway [1].

Gcn1 mutant mice lacking the GCN2-binding domain suffer from growth retardation and postnatal lethality via GCN2-independent mechanisms, while Gcn1-null mice die early in embryonic development. Inducible systemic Gcn1 deletion in adult mice using tamoxifen-inducible conditional knockout (CKO) mice led to transient body weight loss during tamoxifen treatment. This was associated with a decrease in fat and liver glycogen storage, along with changes in hepatic lipid metabolism [2].

In conclusion, Gcn1 is crucial for integrated stress responses and translation quality control. Mouse models, especially KO and CKO mouse models, have revealed its role in growth, development, and metabolic processes such as hepatic lipid metabolism. Understanding Gcn1's functions may offer insights into diseases related to stress responses and metabolic disorders.