CNOT1, a member of the CCR4-NOT complex, is a master regulator in gene expression, RNA deadenylation, and protein ubiquitination [1]. This complex functions in the cytoplasm as the main mRNA deadenylase in constitutive and regulated mRNA decay pathways [3]. CNOT1, encoding the scaffold protein of the CCR4-NOT deadenylase complex, is involved in multiple biological processes, such as brain development, circadian rhythm regulation, and pancreatic development [1,2,4]. Genetic models like Drosophila and mouse models have been crucial for studying its functions.

In Drosophila, knockdown of CNOT1 led to learning and memory defects, and human wild-type CNOT1 could rescue this phenotype, suggesting that CNOT1 impairment causes neurodevelopmental delay [1]. In mice, CNOT1 deficiency resulted in circadian period lengthening and alterations in the mRNA and protein expression patterns of clock genes, mainly Per2, indicating its role in regulating the mammalian circadian clock [2].

In conclusion, CNOT1 is essential in various biological processes. Model-based research, especially the use of Drosophila and mouse models, has revealed its key role in neurodevelopmental delay and circadian behavior regulation. Understanding CNOT1 functions can provide insights into the underlying mechanisms of related diseases and potentially offer new therapeutic targets.