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Molecular and Cellular Biology, August 2002, p. 5585-5592, Vol. 22, No. 15
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.15.5585-5592.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Mice Lacking Paternally Expressed Pref-1/Dlk1 Display Growth Retardation and Accelerated Adiposity

Yang Soo Moon, Cynthia M. Smas,,{dagger} Kichoon Lee, Josep A. Villena, Kee-Hong Kim, Eun Jun Yun, and Hei Sook Sul*

Department of Nutritional Sciences and Toxicology, University of California, Berkeley, California 94720

Received 15 November 2001/ Returned for modification 29 January 2002/ Accepted 24 April 2002

Preadipocyte factor 1 (Pref-1/Dlk1) inhibits in vitro adipocyte differentiation and has been recently reported to be a paternally expressed imprinted gene at human chromosome 14q32. Studies on human chromosome 14 deletions and maternal uniparental disomy (mUPD) 14 suggest that misexpression of a yet-to-be-identified imprinted gene or genes present on chromosome 14 causes congenital disorders. We generated Pref-1 knockout mice to assess the role of Pref-1 in growth and in vivo adipogenesis and to determine the contribution of Pref-1 in mUPD. Pref-1-null mice display growth retardation, obesity, blepharophimosis, skeletal malformation, and increased serum lipid metabolites. Furthermore, the phenotypes observed in Pref-1-null mice are present in heterozygotes that harbor a paternally inherited, but not in those with a maternally inherited pref-1-null allele. Our results demonstrate that Pref-1 is indeed paternally expressed and is important for normal development and for homeostasis of adipose tissue mass. We also suggest that Pref-1 is responsible for most of the symptoms observed in mouse mUPD12 and human mUPD14. Pref-1-null mice may be a model for obesity and other pathologies of human mUPD14.

* Corresponding author. Mailing address: Department of Nutritional Sciences and Toxicology, University of California, Berkeley, CA 94720. Phone: (510) 642-3978. Fax: (510) 642-0535. E-mail: hsul{at}nature.berkeley.edu.

{dagger} Present address: Department of Biochemistry and Molecular Biology, Medical College of Ohio, Toledo, OH 43614.

Molecular and Cellular Biology, August 2002, p. 5585-5592, Vol. 22, No. 15
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.15.5585-5592.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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