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© The Rockefeller University Press, 0021-9525/2000/1/189/ $5.00
The Journal of Cell Biology, Volume 148, Number 1, January 10, 2000 189-202

Original Article

Selective Uncoupling of p120ctn from E-cadherin Disrupts Strong Adhesion

Molly A. Thoresona, Panos Z. Anastasiadisa, Juliet M. Daniela, Reneé C. Iretona, Margaret J. Wheelockb, Keith R. Johnsonb, Diana K. Hummingbirda, and Albert B. Reynoldsa
a Department of Cell Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2175
b Department of Biology, University of Toledo, Toledo, Ohio 43606

Correspondence to: Albert B. Reynolds, Department of Cell Biology, Vanderbilt University, MCN C-2310, Nashville, TN 37232-2175. Tel:(615) 343-9532 Fax:(615) 343-4539 E-mail:al.reynolds{at}mcmail.vanderbilt.edu.

p120ctn is a catenin whose direct binding to the juxtamembrane domain of classical cadherins suggests a role in regulating cell–cell adhesion. The juxtamembrane domain has been implicated in a variety of roles including cadherin clustering, cell motility, and neuronal outgrowth, raising the possibility that p120 mediates these activities. We have generated minimal mutations in this region that uncouple the E-cadherin–p120 interaction, but do not affect interactions with other catenins. By stable transfection into E-cadherin–deficient cell lines, we show that cadherins are both necessary and sufficient for recruitment of p120 to junctions. Detergent-free subcellular fractionation studies indicated that, in contrast to previous reports, the stoichiometry of the interaction is extremely high. Unlike {alpha}- and ß-catenins, p120 was metabolically stable in cadherin-deficient cells, and was present at high levels in the cytoplasm. Analysis of cells expressing E-cadherin mutant constructs indicated that p120 is required for the E-cadherin–mediated transition from weak to strong adhesion. In aggregation assays, cells expressing p120-uncoupled E-cadherin formed only weak cell aggregates, which immediately dispersed into single cells upon pipetting. As an apparent consequence, the actin cytoskeleton failed to insert properly into peripheral E-cadherin plaques, resulting in the inability to form a continuous circumferential ring around cell colonies. Our data suggest that p120 directly or indirectly regulates the E-cadherin–mediated transition to tight cell–cell adhesion, possibly blocking subsequent events necessary for reorganization of the actin cytoskeleton and compaction.

Key Words: metastasis, catenin, compaction, clustering, adherens junction


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