Tfap2b, a pivotal transcription factor, is involved in multiple biological processes. It acts within neural crest cells and their derived lineages, playing critical roles in development [4]. In mammals, it is associated with pathways related to brain development, pigment cell formation, and gastrointestinal function [1,2,3]. Genetic models, such as KO/CKO mouse models, are valuable tools for studying its functions.

In mice, heterozygous deletion of Tfap2b reduces sleep. Further studies revealed that Tfap2b in GABAergic neurons is required for normal sleep, as specific deletion in these neurons led to shortened NREM and REM sleep time and reduced delta and theta power [1]. In zebrafish, disruption of tfap2b led to decreased enteric neuronal numbers, delayed transit time, and decreased levels of ednrbb mRNA, suggesting its role in gastrointestinal development and function [3].

In conclusion, Tfap2b is essential for normal sleep regulation through its action in GABAergic neurons and for proper gastrointestinal function as demonstrated by mouse and zebrafish models. These model-based studies contribute to understanding its role in sleep-related disorders and pediatric intestinal pseudo-obstruction.