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Cell cycle-regulated phosphorylation of p21-activated kinase 1

Debra A Thiel1, Melissa K Reeder, Amanda Pfaff

  • 1Fox Chase Cancer Center, Philadelphia, PA 19111, USA.

Current Biology : CB
|August 15, 2002
PubMed

Insights

Mammalian p21-activated kinase 1 (Pak1) undergoes mitotic phosphorylation by Cdc2 at Thr 212. This phosphorylation impacts fibroblast morphology post-division by altering Pak1

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Mammalian p21-activated kinase 1 (Pak1) is a key effector of Cdc42 and Rac1 small GTPases.
  • Pak1 homologs in lower eukaryotes are regulated by cell cycle-dependent phosphorylation.
  • The role of Pak1 phosphorylation in mammalian cell cycle regulation remains largely unexplored.

Purpose of the Study:

  • To investigate the cell cycle-dependent regulation of mammalian Pak1.
  • To identify the specific site and kinase responsible for Pak1 phosphorylation during mitosis.
  • To elucidate the functional consequences of Pak1 mitotic phosphorylation on cell behavior.

Main Methods:

  • Phosphorylation site mapping in mitotic mammalian fibroblasts.
  • In vitro kinase assays using Cdc2 and Pak1.
  • Site-directed mutagenesis to create phosphomimic Pak1 mutants.
  • Analysis of fibroblast spreading rates and co-immunoprecipitation assays.

Main Results:

  • Pak1 is phosphorylated at a single site, Thr 212, during mitosis in mammalian cells.
  • Cdc2 directly phosphorylates Pak1 at Thr 212 in vitro and is responsible for its mitotic phosphorylation in vivo.
  • A phosphomimetic mutation at Thr 212 significantly alters postmitotic fibroblast spreading and affects Pak1's association with binding partners.

Conclusions:

  • Mammalian Pak1 is a novel cell cycle-regulated protein, phosphorylated by Cdc2 during mitosis.
  • Mitotic phosphorylation of Pak1 at Thr 212 influences cell morphology and dynamics post-division.
  • Pak1's altered interactions with binding partners upon phosphorylation suggest a role in mediating cell division-related morphologic changes.

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