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MyosinV controls PTEN function and neuronal cell size

Michiel T van Diepen1, Maddy Parsons, C Peter Downes

  • 1MRC Centre for Developmental Neurobiology, New Hunt's House, King's College London, London SE1 1UL, UK.

Nature Cell Biology
|September 22, 2009
PubMed

Insights

The tumor suppressor PTEN regulates cell growth by interacting with myosin V motor proteins. This myosin-based transport mechanism is crucial for controlling PTEN

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • PTEN is a tumor suppressor that inhibits cell proliferation, migration, and growth.
  • PTEN acts as a lipid phosphatase, antagonizing phosphoinositide 3-kinase (PI3K) signaling pathways.
  • Mechanisms regulating PTEN's translocation to the cell membrane for activity are not fully understood.

Purpose of the Study:

  • To investigate the role of motor proteins in regulating PTEN function and PI3K signaling.
  • To identify novel interactions and mechanisms controlling PTEN localization and activity.

Main Methods:

  • Förster resonance energy transfer (FRET) measurements to detect protein interactions.
  • Investigating PTEN phosphorylation by CK2 and GSK3.
  • Assessing the impact of myosin V inactivation on neuronal cell size and PI3K/mTor signaling.

Main Results:

  • PTEN directly interacts with myosin V, a motor protein.
  • This interaction is dependent on PTEN phosphorylation by CK2 and/or GSK3.
  • Inactivating myosin V's transport function in neurons led to increased cell size, dependent on PI3K and mTor.

Conclusions:

  • A novel myosin V-based transport mechanism regulates PTEN function.
  • This mechanism plays a critical role in controlling cell growth by modulating PI3K signaling.
  • Findings provide new insights into signaling networks governing cell size and tumor suppression.

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