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Human Molecular Genetics Advance Access published online on September 28, 2007
Human Molecular Genetics, doi:10.1093/hmg/ddm278
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© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Adipose tissue mass is modulated by SLUG (SNAI2)

Pedro Antonio Pérez-Mancera1, Camino Bermejo-Rodríguez1, Inés González-Herrero1, Michel Herranz1, Teresa Flores2, Rafael Jiménez3 and Isidro Sánchez-García1,*

1 Experimental Therapeutics and Translational Oncology Program, Instituto de Biología Moleculary Celular del Cáncer (IBMCC), CSIC/ Universidad de Salamanca, Campus M. Unamuno, 37007-SALAMANCA ( SPAIN) 2 Servicio de Anatomía Patológica, Universidad de Salamanca 3 Departamento de Fisiologíay Farmacología, Universidad de Salamanca

* To whom correspondence should be addressed. Phone: +34-923-238403, Fax: +34-923-294813 E-mail: isg{at}usal.es

Received July 13, 2007; Revised September 5, 2007; Accepted September 19, 2007

The zinc-finger transcription factor SLUG(SNAI2) triggers epithelial-mesenchymal transitions (EMT) and plays an important role in developmental processes. Here we show that SLUG is expressed in white adipose tissue (WAT) in humans and its expression is tightly controlled during adipocyte differentiation. Slug-deficient mice exhibit a marked deficiency in WAT size and Slug-overexpressing mice (Combi-Slug) exhibit an increase in WAT size. Consistent with in vivo data, Slug-deficient MEFs showed a dramatically reduced capacity for adipogenesis in vitro and there was extensive lipid accumulation in Combi-Slug MEFs. The analysis of adipogenic gene expression both in vivo and in vitro showed that PPAR{gamma}2 expression was altered. Complementation studies rescued this phenotype, indicating that WAT alterations induced by Slug are reversible. Our results further show a differential HDAC recruitment to the PPAR{gamma}2 promoter in a tissue- and Slug-dependent manner. Our results connect for the first time adipogenesis with the requirement of a critical level of an EMT regulator in mammals. This work may lead to the development of targeted drugs for treatment of patients with obesity and/or lipodistrophy.


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