Mio depletion links mTOR regulation to Aurora A and Plk1 activation at mitotic centrosomes

Melpomeni Platani (Lead / Corresponding author), Laura Trinkle-Mulcahy, Michael Porter, A. Arockia Jeyaprakash, William C. Earnshaw

    Research output: Contribution to journalArticlepeer-review

    19 Citations (Scopus)


    Coordination of cell growth and proliferation in response to nutrient supply is mediated by mammalian target of rapamycin (mTOR) signaling. In this study, we report that Mio, a highly conserved member of the SEACAT/GATOR2 complex necessary for the activation of mTORC1 kinase, plays a critical role in mitotic spindle formation and subsequent chromosome segregation by regulating the proper concentration of active key mitotic kinases Plk1 and Aurora A at centrosomes and spindle poles. Mio-depleted cells showed reduced activation of Plk1 and Aurora A kinase at spindle poles and an impaired localization of MCAK and HURP, two key regulators of mitotic spindle formation and known substrates of Aurora A kinase, resulting in spindle assembly and cytokinesis defects. Our results indicate that a major function of Mio in mitosis is to regulate the activation/deactivation of Plk1 and Aurora A, possibly by linking them to mTOR signaling in a pathway to promote faithful mitotic progression.

    Original languageEnglish
    Pages (from-to)45-62
    Number of pages18
    JournalJournal of Cell Biology
    Issue number1
    Publication statusPublished - 6 Jul 2015


    • Amino acid sequence
    • Aurora kinase A
    • Cell cycle proteins
    • Centrosome
    • Enzyme activation
    • Gene knockdown techniques
    • HeLa cells
    • Humans
    • Kinesin
    • Mitosis
    • Molecular sequence data
    • Neoplasm proteins
    • Nuclear pore complex proteins
    • Protein structure, Tertiary
    • Protein transport
    • Protein-serine-threonine kinases
    • Proto-oncogene proteins
    • Spindle apparatus
    • TOR serine-threonine kinases


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