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

Author

Listed:
  • 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
    Cell-cell Communication Laboratory, Vascular Pathophysiology Area, Centro Nacional Investigaciones Cardiovasculares (CNIC))

  • Francisco Sánchez-Madrid

    (Servicio de Inmunología, Hospital Universitario de la Princesa, Instituto Investigación Sanitaria Princesa (IIS-IP), Universidad Autónoma de Madrid
    Cell-cell Communication Laboratory, Vascular Pathophysiology Area, Centro Nacional Investigaciones Cardiovasculares (CNIC))

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.

Suggested Citation

  • 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, 2016. "Aurora A drives early signalling and vesicle dynamics during T-cell activation," Nature Communications, Nature, vol. 7(1), pages 1-16, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11389
    DOI: 10.1038/ncomms11389
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