Par-1 promotes a hepatic mode of apical protein trafficking in MDCK cells

David Cohen, Enrique Rodrigues-Boulan, Anne Muesch

Research output: Contribution to journalArticle

41 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)13792-13797
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume101
Issue number38
DOIs
StatePublished - Sep 21 2004
Externally publishedYes

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Madin Darby Canine Kidney Cells
Protein Transport
Hepatocytes
Liver
Epithelial Cells
Caenorhabditis elegans
Golgi Apparatus
Morphogenesis
Blood Proteins
Membrane Proteins
Proteins
Cell Membrane
Kidney
Cell Line
Membranes
Genes

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Par-1 promotes a hepatic mode of apical protein trafficking in MDCK cells. / Cohen, David; Rodrigues-Boulan, Enrique; Muesch, Anne.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 101, No. 38, 21.09.2004, p. 13792-13797.

Research output: Contribution to journalArticle

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