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This version published online on November 21, 2007
Molecular Endocrinology, doi:10.1210/me.2007-0277
Molecular Endocrinology Vol. 0, No. 2007 200702771-
doi:10.1210/me.2007-0277
Copyright © 2007 by the Endocrine Society.
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Submitted on May 31, 2007
Accepted on November 14, 2007

Calcineurin Primes Immature GnRH-Secreting Neuroendocrine Cells for Migration

R. Zaninetti, S. Tacchi, J. Erriquez, C. Distasi, R. Maggi, A. Cariboni, F. Condorelli, P. L. Canonico, and A. A. Genazzani*

Dipartimento di Scienze Chimiche, Alimentari, Farmaceutiche e Farmacologiche and Drug and Food Biotechnology Center, Università degli Studi del Piemonte Orientale "A. Avogadro", Via Bovio 6, 28100 Novara, Italy, and Department of Endocrinology, Center of Excellence on Neurodegenerative Diseases, University of Milan, Milan, Italy

* To whom correspondence should be addressed. E-mail: Genazzani{at}pharm.unipmn.it.

During development, many neurons display calcium-dependent migration, but the role of this messenger in regulating gene expression leading to this event has not yet been elucidated. Among the decoders of calcium signals is calcineurin, a Ca2+/CaM serine/threonine phosphatase that has been involved in both short term and long-term cellular changes. By using immortalised GnRH-secreting neurons, we now show that, in vitro, Ca2+-dependent gene expression, proceeding via calcineurin and the transcription factor NFAT, is a key player controlling the chemomigratory potential of developing GnRH-secreting neurons. Furthermore, our data highlight the "switch" nature of this phosphatase, whose activation or inactivation guides cells to proceed from one genetic program to the next.


Key words: calcineurin • calcium • NFAT • development • GnRH • migration







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