Letter abstract
Nature Cell Biology 10, 1076 - 1082 (2008)
Published online: 10 August 2008 | doi:10.1038/ncb1767
Plk1-dependent phosphorylation of FoxM1 regulates a transcriptional programme required for mitotic progression
Zheng Fu1,3, Liviu Malureanu2,3, Jun Huang4, Wei Wang5, Hao Li5, Jan M. van Deursen2,3, Donald J. Tindall1 & Junjie Chen4
Proper control of entry into and progression through mitosis is essential for normal cell proliferation and the maintenance of genome stability1, 2, 3, 4. The mammalian mitotic kinase Polo-like kinase 1 (Plk1) is involved in multiple stages of mitosis5. Here we report that Forkhead Box M1 (FoxM1), a substrate of Plk1 (refs 6, 7, 8), controls a transcriptional programme that mediates Plk1-dependent regulation of cell-cycle progression. The carboxy-terminal domain of FoxM1 binds Plk1, and phosphorylation of two key residues in this domain by Cdk1 is essential for Plk1–FoxM1 interaction. Formation of the Plk1–FoxM1 complex allows for direct phosphorylation of FoxM1 by Plk1 at G2/M and the subsequent activation of FoxM1 activity, which is required for expression of key mitotic regulators, including Plk1 itself. Thus, Plk1-dependent regulation of FoxM1 activity provides a positive-feedback loop ensuring tight regulation of transcriptional networks essential for orderly mitotic progression.
- Urology and Molecular Biology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.
- Pediatrics and Molecular Biology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
- Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
- Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, Connecticut 06520-8040, USA.
- Department of Chemistry and Chemical Biology, University of New Mexico, Albuquerque, New Mexico 87131, USA.
Correspondence to: Junjie Chen4 e-mail: junjie.chen@yale.edu
Correspondence to: Donald J. Tindall1 e-mail: tindall.donald@mayo.edu
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