Sci. Signal., 15 April 2008
Cell Migration Balancing Stability and Dynamics
Annalisa M. VanHook
Science Signaling, AAAS, Washington, DC 20005, USA
During collective migration events, groups of cells must balance adhesion to one another with the ability to make and break contacts with the substrate. Border cell migration in Drosophila oogenesis is a collective migration in which six to eight cells delaminate from the epithelium surrounding the egg chamber and migrate as a cluster to the anterior end of the oocyte. New studies from Melani et al. and Llense and Martín-Blanco show that the Jun N-terminal kinase (JNK) and signal transducer and activator of transcription (STAT) signaling pathways are required to fine-tune the balance between adhesion and migration in border cells. In the first study, Melani et al. found that border cells lacking Hindsight (Hnt), a transcription factor that inhibits JNK signaling, failed to delaminate and had greater than normal amounts of the adhesion proteins Armadillo (Arm, a β-catenin homolog) and DE-Cadherin (Cad) on their surfaces. When Hnt was overexpressed in border cells, the amount of Arm and Cad on the cell surfaces was less than normal, and the clusters dissociated so completely that migration failed. The Llense and Martín-Blanco study found that JNK signaling modulated abundance of the adherens junction component Bazooka and the cytoskeletal adapter D-Paxillin in border cells. Both studies showed that mutations in JNK pathway components caused border cell clusters to dissociate without completely disrupting their migration, indicating that precise control of JNK signaling is required to regulate adhesion between border cells but not between the border cells and the substrate. Melani et al. also determined that Hnt overexpression reduced STAT activation in the border cells, and mutations in STAT pathway components caused migration defects without dissociation. Finally, the authors demonstrated that the human homolog of Hnt was required for collective migration of breast epithelial cells in a wound-healing assay. These papers provide evidence that the JNK and STAT signaling pathways contribute to distinct aspects of collective migration and that the strength of adhesion between migrating cells is proportional to JNK signaling activity.
M. Melani, K. J. Simpson, J. S. Brugge, D. Montell, Regulation of cell adhesion and collective cell migration by Hindsight and its human homolog RREB1. Curr. Biol. 18, 532-537 (2008). [PubMed]
F. Llense, E. Martín-Blanco, JNK signaling controls border cell cluster integrity and collective cell migration. Curr. Biol. 18, 538-544 (2008). [PubMed]
Citation: A. M. VanHook, Balancing Stability and Dynamics. Sci. Signal. 1, ec133 (2008).
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