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Published online 16 October 2006. doi:10.1083/jcb.200602125
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 175, Number 2, 337-347
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Article

Endosomes generate localized Rho–ROCK–MLC2–based contractile signals via Endo180 to promote adhesion disassembly



Justin Sturge, Dirk Wienke, and Clare M. Isacke

Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, London SW3 6JB, England, UK

Correspondence to Clare M. Isacke: clare.isacke{at}icr.ac.uk

The regulated assembly and disassembly of focal adhesions and adherens junctions contributes to cell motility and tumor invasion. Pivotal in this process is phosphorylation of myosin light chain-2 (MLC2) by Rho kinase (ROCK) downstream of Rho activation, which generates the contractile force necessary to drive disassembly of epithelial cell–cell junctions and cell–matrix adhesions at the rear of migrating cells. How Rho–ROCK–MLC2 activation occurs at these distinct cellular locations is not known, but the emerging concept that endocytic dynamics can coordinate key intracellular signaling events provides vital clues. We report that endosomes containing the promigratory receptor Endo180 (CD280) can generate Rho–ROCK–MLC2–based contractile signals. Moreover, we provide evidence for a cellular mechanism in which Endo180-containing endosomes are spatially localized to facilitate their contractile signals directly at sites of adhesion turnover. We propose migration driven by Endo180 as a model for the spatial regulation of contractility and adhesion dynamics by endosomes.

J. Sturge's present address is Prostate Cancer Research Group, Department of Medical Oncology, Division of Surgery, Oncology, Reproductive Biology and Anaesthesia, Faculty of Medicine, Imperial College London, Hammersmith Hospital Campus, London, W12 0NN, UK.

D. Wienke's present address is Oncology Research NCE, Global Preclinical Research and Development, Merck KGaA, 64293 Darmstadt, Germany.

Abbreviations used in this paper: EEA1, early endosome antigen 1; LDL, low-density lipoprotein; LDLR, LDL receptor; LIMK, LIM kinase; MLC, myosin light chain; MYPT, myosin phosphatase; ROCK, Rho kinase; uPA, urokinase-type plasminogen activator; uPAR, uPA receptor.


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