Presentation Details
| Fezf1 is Required for the Proper Development of the Terminal Nerve of Rodents. Enrico Amato1, 2, 3, Ed Zandro M Taroc1, 2, 3, Paolo E Forni1, 2, 3. 1Department of Biological Sciences, University at Albany, State University of New York, Albany, NY, USA.2The RNA Institute, University at Albany, State University of New York, Albany, NY, USA.3The Center for Neuroscience Research, University at Albany, State University of New York, Albany, NY, USA |
Abstract
The nasal placode (NP) gives rise to diverse neurons, including olfactory, vomeronasal, Gonadotropin-releasing hormone-1 (GnRH-1), and terminal nerve (TN)/pioneer neurons. The GnRH-1 neurons are essential for regulating the hypothalamic-gonadal (HPG) axis, influencing puberty and fertility. During embryonic development in mammals, the GnRH-1 neurons migrate from the developing vomeronasal organ (VNO) anlage to the hypothalamus along the axonal projections of the TN. In mice, TN neurons express Prokineticin receptor 2 (Prokr2). Genetic tracing experiments indicate that the TN neurons are distinct from olfactory, vomeronasal, and GnRH neurons. Pioneer/TN neurons have been previously implicated in inducing olfactory bulb morphogenesis. Incorrect development and migration of GnRH-1 neurons can lead to hypogonadotropic hypogonadism (HH). HH is clinically defined as Kallman syndrome (KS) when associated with impaired olfactory system development. The transcription factor Fezf1 is crucial for proper olfactory system development. Fezf1 loss-of-function has been linked to KS in human and mouse models. Using Fezf1GFP Knock-in/out reporter mice, we observed that GnRH-1 neurons do not express Fezf1. However, by crossbreeding Fezf1GFP mice with Prokr2cre/R26R we observed that Fezf1 is expressed by the TN neurons. Analyses of ProKr2Cre traced Fezf1 KO suggest cell-autonomous effects of Fezf1 on TN development. Our data provide a new paradigm to comprehend the cellular/molecular etiology of KS in humans.
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No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.