Sociosexual behavior requires both activating and repressive roles of <i>Tfap2e/</i>AP-2ε in vomeronasal sensory neurons.

Abstract

Neuronal identity dictates the position in an epithelium, and the ability to detect, process, and transmit specific signals to specified targets. Transcription factors (TFs) determine cellular identity via direct modulation of genetic transcription and recruiting chromatin modifiers. However, our understanding of the mechanisms that define neuronal identity and their magnitude remain a critical barrier to elucidate the etiology of congenital and neurodegenerative disorders. The rodent vomeronasal organ provides a unique system to examine in detail the molecular mechanisms underlying the differentiation and maturation of chemosensory neurons. Here, we demonstrated that the identity of postmitotic/maturing vomeronasal sensory neurons (VSNs), and vomeronasal-dependent behaviors can be reprogrammed through the rescue of <i>Tfap2e/</i>AP-2ε expression in the <i>Tfap2e^Null</i> mice, and partially reprogrammed by inducing ectopic <i>Tfap2e</i> expression in mature apical VSNs. We suggest that the TF <i>Tfap2e</i> can reprogram VSNs bypassing cellular plasticity restrictions, and that it directly controls the expression of batteries of vomeronasal genes.