Par-1 promotes a hepatic mode of apical protein trafficking in MDCK cells.
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Cohen D, Rodriguez-Boulan E, Musch A
Par-1 promotes a hepatic mode of apical protein trafficking in MDCK cells.
Proc Natl Acad Sci U S A. 2004 Sep 21;101(38):13792-7. Epub 2004 Sep 13.
- PubMed ID
- 15365179 [ View in PubMed]
- Abstract
Simple (i.e., nonstratified) epithelial cells use two different routes to target their newly synthesized luminal plasma membrane proteins to the cell surface: a direct route from the Golgi complex, as in the kidney-derived MDCK cell line, or an indirect route that involves a intermediate stop at the ab-luminal (basolateral) membrane, as in hepatocytes. The mechanisms or proteins responsible for these different protein targeting strategies are not known. Here, we show that increased expression of EMK1, a mammalian ortholog of Caenorhabditis elegans Par-1, in MDCK cells promotes a switch from a direct to a transcytotic mode of apical protein delivery and other trafficking changes typical of hepatocytes. These results, together with our recent demonstration that PAR-1 promotes morphological features of hepatocytes in MDCK cells, indicate that Par-1 modulates the developmental decision to build a columnar versus a hepatic epithelial cell. To our knowledge, Par-1 is the first gene assigned to this task in epithelial morphogenesis.