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Published online September 24, 2007
doi:10.1083/jcb.200705035
The Journal of Cell Biology, Vol. 178, No. 7, 1223-1235
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Wyatt et al.
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Article

 The protein tyrosine phosphatase Pez regulates TGFß, epithelial–mesenchymal transition, and organ development

Leila Wyatt1,2, Carol Wadham1, Lesley A. Crocker1, Michael Lardelli3, and Yeesim Khew-Goodall1,2

1 Hanson Institute, Institute of Medical and Veterinary Science, Adelaide SA 5000, Australia
2 Discipline of Biochemistry and 3 Discipline of Genetics, School of Molecular and Biomedical Science, The University of Adelaide, Adelaide 5005, Australia

Correspondence to Yeesim Khew-Goodall: yeesim.khew-goodall{at}imvs.sa.gov.au

Epithelial–mesenchymal transition (EMT), crucial during embryogenesis for new tissue and organ formation, is also considered to be a prerequisite to cancer metastasis. We report here that the protein tyrosine phosphatase Pez is expressed transiently in discrete locations in developing brain, heart, pharyngeal arches, and somites in zebrafish embryos. We also find that Pez knock-down results in defects in these organs, indicating a crucial role in organogenesis. Overexpression of Pez in epithelial MDCK cells causes EMT, with a drastic change in cell morphology and function that is accompanied by changes in gene expression typical of EMT. Transfection of Pez induced TGFß signaling, critical in developmental EMT with a likely role also in oncogenic EMT. In zebrafish, TGFß3 is co- expressed with Pez in a number of tissues and its expression was lost from these tissues when Pez expression was knocked down. Together, our data suggest Pez plays a crucial role in organogenesis by inducing TGFß and EMT.

Abbreviations used in this paper: AJ, adherens junction; A-V, atrio-ventricular; EMT, epithelial–mesenchymal transition; hpf, hours post-fertilization; MO, morpholino oligonucleotide; PTP, protein tyrosine phosphatase.


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