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Published 18 December 2006. doi:10.1083/jcb.200607025
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 175, Number 6, 861-868
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p14–MP1-MEK1 signaling regulates endosomal traffic and cellular proliferation during tissue homeostasis



David Teis1, Nicole Taub1, Robert Kurzbauer5, Diana Hilber1, Mariana E. de Araujo1, Miriam Erlacher2, Martin Offterdinger1, Andreas Villunger2, Stephan Geley3, Georg Bohn6, Christoph Klein6, Michael W. Hess4, and Lukas A. Huber1

1 Division of Cell Biology, 2 Division of Experimental Pathophysiology and Immunology, and 3 Division of Molecular Pathophysiology, Biocenter, and 4 Department of Anatomy, Histology, and Embryology, Innsbruck Medical University, A-6020 Innsbruck, Austria
5 Institute of Molecular Pathology, 1-1030 Vienna, Austria
6 Department of Pediatric Hematology and Oncology, Hannover Medical School, D-30625 Hannover, Germany

Correspondence to Lukas A. Huber: Lukas.A.Huber{at}i-med.ac.at

The extracellular signal-regulated kinase (ERK) cascade regulates proliferation, differentiation, and survival in multicellular organisms. Scaffold proteins regulate intracellular signaling by providing critical spatial and temporal specificity. The scaffold protein MEK1 (mitogen-activated protein kinase and ERK kinase 1) partner (MP1) is localized to late endosomes by the adaptor protein p14. Using conditional gene disruption of p14 in mice, we now demonstrate that the p14–MP1-MEK1 signaling complex regulates late endosomal traffic and cellular proliferation. This function its essential for early embryogenesis and during tissue homeostasis, as revealed by epidermis-specific deletion of p14. These findings show that endosomal p14–MP1-MEK1 signaling has a specific and essential function in vivo and, therefore, indicate that regulation of late endosomal traffic by extracellular signals is required to maintain tissue homeostasis.

D. Teis and N. Taub contributed equally to this paper.

Abbreviations used in this paper: EGFR, EGF receptor; ERK, extracellular signal-regulated kinase; KSR, kinase suppressor of Ras; LBPA, lysobisphosphatidic acid; MEF, mouse embryonic fibroblast; MEK, MAPK and ERK kinase; MORE, Mox2Cre; MP1, MEK1 partner; MVB, multivesicular body; RAF, Ras-activated factor; wt, wild type.


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