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The Polarity Protein Par1b/EMK/MARK2 Regulates T Cell Receptor-Induced Microtubule-Organizing Center Polarization¹

Joseph Lin^*, Kirk K. Hou^*, Helen Piwnica-Worms^, and Andrey S. Shaw^*,,2

*Department of Pathology and Immunology, Department of Cell Biology and Physiology, and Howard Hughes Medical Institute, Washington University School of Medicine, Saint Louis, MO 63110

Engagement of a T cell to an APC induces the formation of an immunological synapse as well as reorientation of the microtubule-organizing center (MTOC) toward the APC. How signals emanating from the TCR induce MTOC polarization is not known. One group of proteins known to play a critical role in asymmetric cell division and cell polarization is the partitioning defective (Par) family of proteins. In this study we found that Par1b, a member of the Par family of proteins, was inducibly phosphorylated following TCR stimulation. This phosphorylation resulted in 14-3-3 protein binding and caused the relocalization of Par1b from the membrane into the cytoplasm. Because a dominant-negative form of Par1b blocked TCR-induced MTOC polarization, our data suggest that Par1b functions in the establishment of T cell polarity following engagement to an APC.

² Address correspondence and reprint requests to Dr. Andrew S. Shaw, Department of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid, Box 8118, Saint Louis, MO. E-mail address: shaw{at}pathology.wustl.edu

¹ J.L. is supported by a Cancer Research Institute Postdoctoral Fellowship.