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Originally published as MBC in Press, 10.1091/mbc.E06-07-0651 on December 20, 2006

Vol. 18, Issue 3, 874-885, March 2007

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PALS1 Regulates E-Cadherin Trafficking in Mammalian Epithelial CellsFormula

Qian Wang*, Xiao-Wei Chen{dagger}, and Ben Margolis*,{ddagger}

Departments of *Biological Chemistry, {dagger}Molecular and Integrative Physiology, and {ddagger}Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109

Submitted July 31, 2006; Revised November 14, 2006; Accepted December 7, 2006
Monitoring Editor: Keith Mostov

Protein Associated with Lin Seven 1 (PALS1) is an evolutionarily conserved scaffold protein that targets to the tight junction in mammalian epithelia. Prior work in our laboratory demonstrated that the knockdown of PALS1 in Madin Darby canine kidney cells leads to tight junction and polarity defects. We have created new PALS1 stable knockdown cell lines with more profound reduction of PALS1 expression, and a more severe defect in tight junction formation was observed. Unexpectedly, we also observed a severe adherens junction defect, and both defects were corrected when PALS1 wild type and certain PALS1 mutants were expressed in the knockdown cells. We found that the adherens junction structural component E-cadherin was not effectively delivered to the cell surface in the PALS1 knockdown cells, and E-cadherin puncta accumulated in the cell periphery. The exocyst complex was also found to be mislocalized in PALS1 knockdown cells, potentially explaining why E-cadherin trafficking is disrupted. Our results suggest a broad and evolutionarily conserved role for the tight junction protein PALS1 in the biogenesis of adherens junction.

This was published online ahead of print in MBC in Press (http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E06-07-0651) on December 20, 2006.

Formula The online version of this article contains supplemental material at MBC Online (http://www.molbiolcell.org).

Address correspondence to: Ben Margolis (bmargoli{at}umich.edu)




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