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Role of Fyn in the Rearrangement of Tubulin Cytoskeleton Induced through TCR¹

Noa B. Martín-Cófreces^2,*, David Sancho^2,3,*, Edgar Fernández, Miguel Vicente-Manzanares^*, Mónica Gordón-Alonso^*, María C. Montoya, Frédérique Michel, Oreste Acuto, Balbino Alarcón and Francisco Sánchez-Madrid^4,*

^* Servicio de Inmunología, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain; Confocal Microscopy and Citometry Unit, Biotechnology Program, Centro Nacional de Investigaciones Oncológicas, Madrid, Spain; and Molecular Immunology Unit, Department of Immunology, Institut Pasteur, Paris, France

The translocation of the microtubule-organizing center (MTOC), its associated signaling complex, and the secretory apparatus is the most characteristic early event that involves the tubulin cytoskeleton of T or NK cells after their interaction with APC or target cells. Our results show that Fyn kinase activity is essential for MTOC reorientation in an Ag-dependent system. Moreover, T cells from Fyn-deficient mice are unable to rearrange their tubulin cytoskeleton in response to anti-CD3-coated beads. Analysis of conjugates of T cells from transgenic OT-I mice with dendritic cells revealed that an antagonist peptide induces translocation of the MTOC, and that this process is impaired in T cells from Fyn^–/– OT-I mice. In addition, Fyn deficiency significantly affects the MTOC relocation mediated by agonist peptide stimulation. These results reveal Fyn to be a key regulator of tubulin cytoskeleton reorganization in T cells.

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