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p14-MP1-MEK1 signaling regulates endosomal traffic and cellular proliferation during tissue homeostasis

David Teis1, Nicole Taub, Robert Kurzbauer

  • 1Division of Cell Biology, Innsbruck Medical University, A-6020 Innsbruck, Austria.

The Journal of Cell Biology
|December 21, 2006
PubMed

Insights

The p14-MP1-MEK1 signaling complex on late endosomes controls cell proliferation and endosomal traffic. This pathway is crucial for early embryonic development and maintaining tissue homeostasis in adult organisms.

Area of Science:

  • Cell Biology
  • Molecular Signaling
  • Developmental Biology

Background:

  • Extracellular signal-regulated kinase (ERK) cascade is vital for cell functions.
  • Scaffold proteins like MEK1 partner (MP1) ensure signaling specificity.
  • MP1 is localized to late endosomes by the adaptor protein p14.

Purpose of the Study:

  • To investigate the in vivo function of the p14-MP1-MEK1 signaling complex.
  • To determine the role of this complex in regulating late endosomal traffic and cellular proliferation.

Main Methods:

  • Conditional gene disruption of p14 in mice.
  • Epidermis-specific deletion of p14 to assess tissue homeostasis.

Main Results:

  • The p14-MP1-MEK1 complex regulates late endosomal traffic.
  • This complex is essential for cellular proliferation.
  • Deletion of p14 impairs early embryogenesis and tissue homeostasis.

Conclusions:

  • Endosomal p14-MP1-MEK1 signaling is essential for in vivo functions.
  • Regulation of late endosomal traffic by extracellular signals maintains tissue homeostasis.

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