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Mitogen-activated protein kinase (MAPK/ERK) regulates adenomatous polyposis coli during growth-factor-induced cell

Hector Y Caro-Gonzalez1, Lene N Nejsum, Kathleen A Siemers

  • 1Department of Biology, Stanford University, Stanford, CA 94305-5435, USA.

Journal of Cell Science
|March 9, 2012
PubMed

Insights

Adenomatous polyposis coli (APC) protein phosphorylation is regulated by both GSK-3β inhibition and MAPK/ERK pathway activation during cell extension. This dual regulation controls APC

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Adenomatous polyposis coli (APC) is a microtubule- and actin-binding protein essential for cell extension formation.
  • APC's function is regulated by phosphorylation, particularly by glycogen synthase kinase-3β (GSK-3β), which typically decreases its microtubule-bundling activity.
  • The phosphorylation status of APC during cell extension initiation has not been directly investigated.

Purpose of the Study:

  • To investigate the phosphorylation state of APC during growth factor-induced cell extensions.
  • To elucidate the roles of GSK-3β and the MAPK/ERK pathway in regulating APC's interaction with the cytoskeleton during cell extension.

Main Methods:

  • Analysis of APC phosphorylation in response to Nerve Growth Factor (NGF) and Epidermal Growth Factor (EGF).
  • Investigating the involvement of the MAPK/ERK pathway and GSK-3β.
  • In vitro assays to assess APC's interaction with F-actin and microtubules under different phosphorylation conditions.

Main Results:

  • NGF and EGF induce APC phosphorylation via the MAPK/ERK pathway during initial cell extensions.
  • ERK-mediated phosphorylation inhibits APC's interaction with F-actin and F-actin bundling.
  • GSK-3β inhibition promotes APC binding and microtubule stabilization, while ERK phosphorylation affects F-actin interactions.
  • Both GSK-3β and ERK pathways act in parallel to modulate APC-cytoskeleton interactions.

Conclusions:

  • A novel regulatory pathway for APC involving MAPK/ERK-mediated phosphorylation during cell extension is identified.
  • APC phosphorylation by ERK and inhibition by GSK-3β have distinct, parallel roles in cytoskeletal regulation.
  • These findings provide new insights into the dynamic control of cell extension formation.

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