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J. Biol. Chem., Vol. 280, Issue 30, 27856-27865, July 29, 2005

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A Causative Role of Stromelysin-3 in Extracellular Matrix Remodeling and Epithelial Apoptosis during Intestinal Metamorphosis in Xenopus laevis^*

Liezhen Fu, Atsuko Ishizuya-Oka, Daniel R. Buchholz, Tosikazu Amano, Hiroki Matsuda, and Yun-Bo Shi¶

From the Laboratory of Gene Regulation and Development, NICHD, National Institutes of Health, Bethesda, Maryland 20892 and the Department of Biology, Nippon Medical School, Kawasaki, Kanagawa 211-0063, Japan

The matrix metalloproteinases are a family of proteases capable of degrading various components of the extracellular matrix. Expression studies have implicated the involvement of the matrix metalloproteinase stromelysin-3 (ST3) in tissue remodeling and pathogenesis. However, the in vivo role of ST3 has been difficult to study because of a lack of good animal models. Here we used intestinal remodeling during thyroid hormone-dependent metamorphosis of Xenopus laevis as a model to investigate in vivo the role of ST3 during postembryonic organ development in vertebrates. We generated transgenic tadpoles expressing ST3 under control of a heat shock-inducible promoter. We showed for the first time in vivo that wild type ST3 but not a catalytically inactive mutant was sufficient to induce larval epithelial cell death and fibroblast activation, events that normally occur only in the presence of thyroid hormone. We further demonstrated that these changes in cell fate are associated with altered gene expression in the intestine and remodeling of the intestinal basal lamina. These results thus suggest that ST3 regulates cell fate and tissue morphogenesis through direct or indirect ECM remodeling.

Received for publication, November 24, 2004 , and in revised form, May 26, 2005.

^* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ To whom correspondence should be addressed: Bldg. 18 T, Rm. 106, LGRD, NICHD, National Institutes of Health, Bethesda, MD 20892. Tel.: 301-402-1004; Fax: 301-402-1323; E-mail: Shi{at}helix.nih.gov.

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