Department of Biological Sciences, University at Albany, State University of New York, Albany, United States; The RNA Institute, University at Albany, Albany, United States
Department of Biological Sciences, University at Albany, State University of New York, Albany, United States; The RNA Institute, University at Albany, Albany, United States
Megan Rothstein
Department of Molecular Biology and Genetics, Cornell University, Ithaca, United States
Alison Pehl
Department of Biological Sciences, University at Albany, State University of New York, Albany, United States; The RNA Institute, University at Albany, Albany, United States
Ed Zandro M Taroc
Department of Biological Sciences, University at Albany, State University of New York, Albany, United States; The RNA Institute, University at Albany, Albany, United States
Raghu R Katreddi
Department of Biological Sciences, University at Albany, State University of New York, Albany, United States; The RNA Institute, University at Albany, Albany, United States
Katherine E Parra
Department of Psychology, University at Albany, State University of New York, Albany, United States
Damian G Zuloaga
Department of Psychology, University at Albany, State University of New York, Albany, United States
Department of Biological Sciences, University at Albany, State University of New York, Albany, United States; The RNA Institute, University at Albany, Albany, United States
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 Tfap2e/AP-2ε expression in the Tfap2eNull mice, and partially reprogrammed by inducing ectopic Tfap2e expression in mature apical VSNs. We suggest that the TF Tfap2e can reprogram VSNs bypassing cellular plasticity restrictions, and that it directly controls the expression of batteries of vomeronasal genes.
