Dataset from: Functional divergence of mammalian TFAP2a and TFAP2b transcription factors for bidirectional sleep control

Sleep is a conserved behavioral state that is found in all animals that
have a nervous system. Invertebrates typically show quiet sleep, whereas
in mammals, sleep is more complex, and consists of periods of
non-rapid-eye-movement sleep (NREMS) and REM sleep (REMS). We previously
found that the transcription factor AP-2 is required for sleep in C.
elegans and Drosophila and that the C. elegans AP-2 gene aptf-1 is
required for sleep-active neurons to induce sleep. In mammals, several
paralogous AP-2 transcription factors exist. Sleep-controlling genes are
often conserved. However, little is known about how sleep genes evolved
from controlling simpler types of sleep to govern complex mammalian sleep.
Here, we studied the roles of Tfap2a and Tfap2b in sleep control in mice.
Consistent with our results from C. elegans and Drosophila, the AP-2
transcription factors Tfap2a and Tfap2b also control sleep in mice.
Surprisingly, however, the two AP-2 paralogs play contrary roles in sleep
control. Tfap2a reduction of function causes stronger delta and theta
power in both baseline and homeostasis analysis, thus indicating increased
sleep quality, but did not affect sleep quantity. By contrast, Tfap2b
reduction of function decreased NREM sleep time specifically during the
dark phase, reduced NREMS and REMS power, and caused a weaker response to
sleep deprivation. Consistent with the observed signatures of decreased
sleep quality, stress resistance and memory were impaired in Tfap2b mutant
animals. Also, the circadian period was slightly shortened. Taken
together, AP-2 transcription factors control sleep behavior also in mice,
but the role of the AP-2 genes functionally diversified to allow for a
bidirectional control of sleep quality. Divergence of AP-2 transcription
factors might perhaps have supported the evolution of more complex types
of sleep.