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 journalArticle

8 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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