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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.

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.

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

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

³ Abbreviations used in this paper: MTOC, microtubule-organizing center; aPKC, atypical PKC; KD, kinase dead; MAP, microtubule-associated protein; pS400, phosphorylated serine 400; pT595, phosphorylated threonine 595; Par, partition defective; PFA, paraformaldehyde; nPKC, novel KPCK; PKC, protein kinase C; PKD, protein kinase D; SEE, staphylococcal enterotoxin E; wt, wild type.