| Literature DB >> 14532135 |
Takayuki Okano-Uchida1, Eiichi Okumura, Motoko Iwashita, Hitoshi Yoshida, Kazunori Tachibana, Takeo Kishimoto.
Abstract
The Polo-like kinase, Plk, has multiple roles in regulating mitosis. In particular, Plk1 has been postulated to function as a trigger kinase that phosphorylates and activates Cdc25C prior to the activation of cyclin B-Cdc2 and thereby initiates its activation. However, the upstream regulation of Plk1 activation remains unclear. Here we have studied the interplay between Plk1 and Cdc2 through meiotic and early embryonic cycles in starfish. Distinct kinases, cyclin B-Cdc2, MAPK along with cyclin B- and/or cyclin A-Cdc2 and cyclin A-Cdc2, were unique upstream regulators for Plk1 activation at meiosis I, meiosis II and embryonic M-phase, respectively, indicating that Plk1 is not the trigger kinase at meiotic reinitiation. When Plk1 was required for cyclin B-Cdc2 activation, the action of Plk1 was mediated primarily through suppression of Myt1 rather than through activation of Cdc25. We propose that Plk1 can be activated by either cyclin A- or cyclin B-Cdc2, and its primary target is Myt1.Entities:
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Year: 2003 PMID: 14532135 PMCID: PMC213789 DOI: 10.1093/emboj/cdg535
Source DB: PubMed Journal: EMBO J ISSN: 0261-4189 Impact factor: 11.598