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14-3-3zeta/tau heterodimers regulate Slingshot activity in migrating keratinocytes

Kristina Kligys1, Jun Yao, Dihua Yu

  • 1Department of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, Tarry 8-716, 303 E. Chicago Avenue, Chicago, IL 60611, USA.

Biochemical and Biophysical Research Communications
|April 18, 2009
PubMed

Insights

14-3-3zeta/tau heterodimers regulate Slingshot phosphatase (SSH1) activity in keratinocytes. This interaction is crucial for cytoskeleton remodeling during cell migration, impacting wound healing and metastasis.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Keratinocyte cell migration is vital for wound healing and tumor metastasis.
  • The alpha6beta4 integrin-Rac1 signaling pathway regulates keratinocyte migration via Slingshot phosphatase (SSH) and cofilin.
  • The precise regulation of SSH1 activity remains to be fully elucidated.

Purpose of the Study:

  • To investigate the role of 14-3-3 isoforms in regulating SSH1 activity.
  • To determine how 14-3-3zeta/tau heterodimers interact with SSH1 and affect its function.

Main Methods:

  • Utilized amino and carboxy terminal domains of 14-3-3zeta in keratinocyte assays.
  • Assayed SSH1 activity by measuring cofilin phosphorylation levels.
  • Investigated protein-protein interactions using overexpression of 14-3-3zeta domains.

Main Results:

  • 14-3-3zeta/tau heterodimers bind to SSH1 in the absence of Rac1 signaling.
  • This binding inhibits SSH1 activity, evidenced by increased phosphorylated cofilin.
  • Overexpression of the 14-3-3zeta carboxy terminal domain inhibited 14-3-3tau and SSH1 interaction.

Conclusions:

  • 14-3-3zeta/tau heterodimers are key regulators of SSH1 activity in keratinocytes.
  • These interactions suggest a role for 14-3-3zeta/tau in cytoskeleton remodeling during cell migration.

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