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MBC in Press, published online ahead of print September 15, 2006
Mol. Biol. Cell 10.1091/mbc.E06-04-0306

A more recent version of this article appeared on November 1, 2006 Originally published as MBC in Press, 10.1091/mbc.E06-04-0306 on September 13, 2006
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Submitted on April 13, 2006
Revised on August 22, 2006
Accepted on August 31, 2006

Loss of T-Cell Protein Tyrosine Phosphatase Induces Recycling of the PDGF {beta}-Receptor but Not of the PDGF {alpha}-Receptor

Susann Karlsson,* Katarzyna Kowanetz,*{dagger} Åsa Sandin,{ddagger} Camilla Persson,*{sect} Arne Östman,{ddagger} Carl-Henrik Heldin,* and Carina Hellberg*

*Ludwig Institute for Cancer Research, Uppsala University Biomedical Center, S-751 24 Uppsala, Sweden; {ddagger}Department of Pathology-Oncology, Cancer Center Karolinska, Karolinska Institute, S-171 76 Stockholm, Sweden

Monitoring Editor: Anne Ridley

We have previously shown that the T-cell protein tyrosine phosphatase (TC-PTP) dephosphorylates the platelet-derived growth factor (PDGF) {beta}-receptor. Here we show that the increased PDGF {beta}-receptor phosphorylation in TC-PTP ko mouse embryonic fibroblasts (MEFs) occurs primarily on the cell surface. The increased phosphorylation is accompanied by a TC-PTP-dependent, monensin-sensitive delay in clearance of cell surface PDGF {beta}-receptors and delayed receptor degradation, suggesting PDGF {beta}-receptor recycling. Recycled receptors could also be directly detected on the cell surface of TC-PTP ko MEFs. The effect of TC-PTP depletion was specific for the PDGF {beta}-receptor, since PDGF {alpha}-receptor homodimers were cleared from the cell surface at the same rate in TC-PTP ko MEFs as in wt MEFs. Interestingly, PDGF {alpha}{beta}-receptor heterodimers were recycling. Analysis by confocal microscopy revealed that, in TC-PTP ko MEFs, activated PDGF {beta}-receptors colocalized with Rab4a, a marker for rapid recycling. In accordance with this, transient expression of a dominant negative Rab4a construct increased the rate of clearance of cell surface receptors on TC-PTP ko MEFs. Thus, loss of TC-PTP specifically redirects the PDGF {beta}-receptor toward rapid recycling, which is the first evidence of differential trafficking of PDGF receptor family members.

Present addresses: {dagger}Molecular Oncology Department, Genentech, South San Francisco, CA 94080; {sect}Karolinska Institutet, MBB/SGC, S-171 77 Stockholm, Sweden.

Address correspondence to: Carina Hellberg (Carina.Hellberg{at}LICR.uu.se)




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