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Bora and Aurora-A continue to activate Plk1 in mitosis
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SYSNO ASEP 0436610 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Bora and Aurora-A continue to activate Plk1 in mitosis Author(s) Bruinsma, W. (NL)
Macůrek, Libor (UMG-J) RID, ORCID
Freire, R. (ES)
Lindqvist, A. (NL)
Medema, R.H. (NL)Source Title Journal of Cell Science. - : Company of Biologists - ISSN 0021-9533
Roč. 127, č. 4 (2014), s. 801-811Number of pages 11 s. Language eng - English Country GB - United Kingdom Keywords Aurora-A ; Bora ; Mitosis ; Plk1 Subject RIV EB - Genetics ; Molecular Biology R&D Projects GA13-18392S GA ČR - Czech Science Foundation (CSF) UT WOS 000332114800010 DOI https://doi.org/10.1242/jcs.137216 Annotation Polo-like kinase-1 (Plk1) is required for proper cell division. Activation of Plk1 requires phosphorylation on a conserved threonine in the T-loop of the kinase domain (T210). Plk1 is first phosphorylated on T210 in G2 phase by the kinase Aurora-A, in concert with its cofactor Bora. However, Bora was shown to be degraded prior to entry into mitosis, and it is currently unclear how Plk1 activity is sustained in mitosis. Here we show that the Bora-Aurora-A complex remains the major activator of Plk1 in mitosis. We show that a small amount of Aurora-A activity is sufficient to phosphorylate and activate Plk1 in mitosis. In addition, a fraction of Bora is retained in mitosis, which is essential for continued Aurora-A-dependent T210 phosphorylation of Plk1. We find that once Plk1 is activated, minimal amounts of the Bora-Aurora-A complex are sufficient to sustain Plk1 activity. Thus, the activation of Plk1 by Aurora-A may function as a bistable switch; highly sensitive to inhibition of Aurora-A in its initial activation, but refractory to fluctuations in Aurora-A activity once Plk1 is fully activated. This provides a cell with robust Plk1 activity once it has committed to mitosis. Workplace Institute of Molecular Genetics Contact Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Year of Publishing 2015
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