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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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CDK1 phosphorylation of TAZ in mitosis inhibits its oncogenic activity

Lin Zhang1,2, Xingcheng Chen2, Seth Stauffer2

  • 1Department of Radiation Oncology, Qilu Hospital of Shandong University, Jinan, Shandong, P.R. China.

Oncotarget
|September 17, 2015
PubMed

Insights

Mitotic phosphorylation by CDK1 inactivates the oncogenic transcriptional co-activator with PDZ-binding motif (TAZ). This regulation is critical for TAZ

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Cancer Research

Background:

  • The transcriptional co-activator with PDZ-binding motif (TAZ) is a key effector of the Hippo pathway, regulating cancer and stem cell biology.
  • Hippo signaling primarily inactivates TAZ via phosphorylation at S89.

Purpose of the Study:

  • To investigate a novel regulatory mechanism of TAZ activity linked to its oncogenic functions.
  • To explore the role of mitotic phosphorylation in controlling TAZ activity and oncogenicity.

Main Methods:

  • In vitro and in vivo phosphorylation assays using CDK1.
  • Generation and analysis of non-phosphorylatable TAZ mutants (TAZ-S89A, TAZ-5A).
  • Assessment of TAZ activity in epithelial-mesenchymal transition, anchorage-independent growth, migration, invasion, and transcriptional activity.
  • Evaluation of TAZ-induced spindle, centrosome, and chromosome segregation defects.

Main Results:

  • TAZ is phosphorylated by CDK1 at multiple sites (S90, S105, T326, T346) during the G2/M phase.
  • Mitotic phosphorylation by CDK1 inactivates TAZ's oncogenic functions.
  • The non-phosphorylatable TAZ-5A mutant exhibits enhanced oncogenic activity and transcriptional output compared to TAZ-S89A.
  • TAZ phosphorylation mutants induce significant spindle, centrosome, and chromosome segregation defects.

Conclusions:

  • A new layer of TAZ regulation involving mitotic phospho-regulation by CDK1 is identified.
  • Mitotic phosphorylation of TAZ is critical for controlling its oncogenic potential.
  • Dysregulation of TAZ mitotic phosphorylation may contribute to cancer development and chromosomal instability.
Keywords:
CDK1Hippo pathwayTAZmitotic defectsmitotic phosphorylation

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