Aurora A drives early signalling and vesicle dynamics during T-cell activation

Noelia Blas-Rus, Eugenio Bustos-Morán, Ignacio Pérez de Castro, Guillermo de Cárcer, Aldo Borroto, Emilio Camafeita, Inmaculada Jorge, Jesús Vázquez, Balbino Alarcón, Marcos Malumbres, Noa B. Martín-Cófreces and Francisco Sánchez-Madrid ()
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Noelia Blas-Rus: Servicio de Inmunología, Hospital Universitario de la Princesa, Instituto Investigación Sanitaria Princesa (IIS-IP), Universidad Autónoma de Madrid
Eugenio Bustos-Morán: Cell-cell Communication Laboratory, Vascular Pathophysiology Area, Centro Nacional Investigaciones Cardiovasculares (CNIC)
Ignacio Pérez de Castro: Centro Nacional de Investigaciones Oncológicas (CNIO)
Guillermo de Cárcer: Centro Nacional de Investigaciones Oncológicas (CNIO)
Aldo Borroto: Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid
Emilio Camafeita: Laboratory of Cardiovascular Proteomics, Centro Nacional Investigaciones Cardiovasculares (CNIC)
Inmaculada Jorge: Laboratory of Cardiovascular Proteomics, Centro Nacional Investigaciones Cardiovasculares (CNIC)
Jesús Vázquez: Laboratory of Cardiovascular Proteomics, Centro Nacional Investigaciones Cardiovasculares (CNIC)
Balbino Alarcón: Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid
Marcos Malumbres: Centro Nacional de Investigaciones Oncológicas (CNIO)
Noa B. Martín-Cófreces: Servicio de Inmunología, Hospital Universitario de la Princesa, Instituto Investigación Sanitaria Princesa (IIS-IP), Universidad Autónoma de Madrid
Francisco Sánchez-Madrid: Servicio de Inmunología, Hospital Universitario de la Princesa, Instituto Investigación Sanitaria Princesa (IIS-IP), Universidad Autónoma de Madrid

Nature Communications, 2016, vol. 7, issue 1, 1-16

Abstract: Abstract Aurora A is a serine/threonine kinase that contributes to the progression of mitosis by inducing microtubule nucleation. Here we have identified an unexpected role for Aurora A kinase in antigen-driven T-cell activation. We find that Aurora A is phosphorylated at the immunological synapse (IS) during TCR-driven cell contact. Inhibition of Aurora A with pharmacological agents or genetic deletion in human or mouse T cells severely disrupts the dynamics of microtubules and CD3ζ-bearing vesicles at the IS. The absence of Aurora A activity also impairs the activation of early signalling molecules downstream of the TCR and the expression of IL-2, CD25 and CD69. Aurora A inhibition causes delocalized clustering of Lck at the IS and decreases phosphorylation levels of tyrosine kinase Lck, thus indicating Aurora A is required for maintaining Lck active. These findings implicate Aurora A in the propagation of the TCR activation signal.

Date: 2016
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DOI: 10.1038/ncomms11389

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