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Molecular and Cellular Biology, July 2000, p. 5119-5128, Vol. 20, No. 14
0270-7306/00/$04.00+0

Growth, Adipose, Brain, and Skin Alterations Resulting from Targeted Disruption of the Mouse Peroxisome Proliferator-Activated Receptor beta (delta )

Jeffrey M. Peters,1,* Susanna S. T. Lee,1,dagger Wen Li,2,Dagger Jerrold M. Ward,3 Oksana Gavrilova,4 Carrie Everett,4 Marc L. Reitman,4 Lynn D. Hudson,2 and Frank J. Gonzalez1

Laboratory of Metabolism, National Cancer Institute,1 Laboratory of Developmental Neurogenetics, National Institute of Neurological Disorders and Stroke,2 and Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases,4 National Institutes of Health, Bethesda, Maryland 20892, and Veterinary and Tumor Pathology Section, Office of Laboratory Animal Resources, National Cancer Institute, Frederick, Maryland 217023

Received 18 January 2000/Returned for modification 28 February 2000/Accepted 13 April 2000

To determine the physiological roles of peroxisome proliferator-activated receptor beta  (PPARbeta ), null mice were constructed by targeted disruption of the ligand binding domain of the murine PPARbeta gene. Homozygous PPARbeta -null term fetuses were smaller than controls, and this phenotype persisted postnatally. Gonadal adipose stores were smaller, and constitutive mRNA levels of CD36 were higher, in PPARbeta -null mice than in controls. In the brain, myelination of the corpus callosum was altered in PPARbeta -null mice. PPARbeta was not required for induction of mRNAs involved in epidermal differentiation induced by O-tetradecanoylphorbol-13-acetate (TPA). The hyperplastic response observed in the epidermis after TPA application was significantly greater in the PPARbeta -null mice than in controls. Inflammation induced by TPA in the skin was lower in wild-type mice fed sulindac than in similarly treated PPARbeta -null mice. These results are the first to provide in vivo evidence of significant roles for PPARbeta in development, myelination of the corpus callosum, lipid metabolism, and epidermal cell proliferation.

* Corresponding author. Mailing address: Center for Molecular Toxicology, Department of Veterinary Science, The Pennsylvania State University, 226 Fenske Laboratory, University Park, PA 16802-4401. Phone: (814) 863-1387. Fax: (814) 863-1696. E-mail: jmp21{at}psu.edu.

dagger Present address: Department of Biochemistry, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, China.

Dagger Present address: Neurotoxicology Laboratory, Department of Entomology, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061.

Molecular and Cellular Biology, July 2000, p. 5119-5128, Vol. 20, No. 14
0270-7306/00/$04.00+0


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