# Crucial role of TFAP2B in the nervous system for regulating NREM sleep

## TL;DR

This study shows that the TFAP2B gene in the nervous system is important for regulating NREM sleep and circadian rhythms in mice.

## Contribution

The study identifies the specific role of TFAP2B in neurons for sleep regulation and reveals its impact on circadian clock function.

## Key findings

- Nervous system-specific deletion of Tfap2b in mice caused reduced NREM sleep and severe sleep phenotypes.
- Postnatal neuronal deletion of Tfap2b also reduced NREM sleep but with less severe effects.
- Defective light entrainment of the circadian clock and stereotypic jumping behavior were observed in mice with nervous system-specific Tfap2b deletion.

## Abstract

The AP-2 transcription factors are crucial for regulating sleep in both vertebrate and invertebrate animals. In mice, loss of function of the transcription factor AP-2β (TFAP2B) reduces non-rapid eye movement (NREM) sleep. When and where TFAP2B functions, however, is unclear. Here, we used the Cre-loxP system to generate mice in which Tfap2b was specifically deleted in the nervous system during development and mice in which neuronal Tfap2b was specifically deleted postnatally. Both types of mice exhibited reduced NREM sleep, but the nervous system-specific deletion of Tfap2b resulted in more severe sleep phenotypes accompanied by defective light entrainment of the circadian clock and stereotypic jumping behavior. These findings indicate that TFAP2B in postnatal neurons functions at least partly in sleep regulation and imply that TFAP2B also functions either at earlier stages or in additional cell types within the nervous system.

The online version contains supplementary material available at 10.1186/s13041-024-01084-8.