![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
|
|
|
|
|
||
A more recent version of this article appeared on June 1, 2007
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on February 2, 2007
Revised on March 16, 2007
Accepted on March 28, 2007
*The Margaret Dyson Institute of Vision Research and Graduate Program in Physiology, Biophysics and Systems Biology, Weill Medical College of Cornell University, New York, NY 10021
Monitoring Editor: Keith Mostov
Kidney-derived MDCK cells form lumina at their apices, and target luminal proteins to an intracellular vacuolar apical compartment (VAC) when prevented from polarizing. Hepatocytes, by contrast, organize their luminal surfaces (the bile canaliculi, BC) between their lateral membranes and, when nonpolarized, display an intracellular luminal compartment that is distinct from the VACs of MDCK cells. Overexpression of the serine/threonine kinase Par1b/EMK1/MARK2 induces BC-like lateral lumina and a hepatic-type intracellular luminal compartment in MDCK cells, suggesting a role for Par1b in the branching decision between kidney-and hepatic-type epithelial phenotypes. Here, we report that Par1b promotes lateral lumen polarity in MDCK cells independent of Ca-mediated cell-cell adhesion by inhibiting myosin II in a rho-kinase dependent manner. Polarization was inhibited by E-cadherin depletion but promoted by an adhesion-defective E-cadherin mutant. By contrast, apical surface formation in control MDCK cells required Ca-dependent cell-cell adhesion but occurred in the absence of E-cadherin. We propose that E-cadherin, when in an adhesion-incompetent state at the lateral domain, serves as targeting patch for the establishment of lateral luminal surfaces. E-cadherin depletion also reverted the hepatic-type intracellular luminal compartment in Par1b-MDCK cells to VACs characteristic of control MDCK cells, indicating a novel link between E-cadherin and luminal protein targeting.
This article has been cited by other articles:
|
|
 |
|
  M. Desclozeaux, J. Venturato, F. G. Wylie, J. G. Kay, S. R. Joseph, H. T. Le, and J. L. Stow Active Rab11 and functional recycling endosome are required for E-cadherin trafficking and lumen formation during epithelial morphogenesis Am J Physiol Cell Physiol, August 1, 2008; 295(2): C545 - C556. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Sapir, S. Sapoznik, T. Levy, D. Finkelshtein, A. Shmueli, T. Timm, E.-M. Mandelkow, and O. Reiner Accurate Balance of the Polarity Kinase MARK2/Par-1 Is Required for Proper Cortical Neuronal Migration J. Neurosci., May 28, 2008; 28(22): 5710 - 5720. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. F. Hezel, S. Gurumurthy, Z. Granot, A. Swisa, G. C. Chu, G. Bailey, Y. Dor, N. Bardeesy, and R. A. DePinho Pancreatic Lkb1 Deletion Leads to Acinar Polarity Defects and Cystic Neoplasms Mol. Cell. Biol., April 1, 2008; 28(7): 2414 - 2425. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. T. Braiterman, S. Heffernan, L. Nyasae, D. Johns, A. P. See, R. Yutzy, A. McNickle, M. Herman, A. Sharma, U. P. Naik, et al. JAM-A is both essential and inhibitory to development of hepatic polarity in WIF-B cells Am J Physiol Gastrointest Liver Physiol, February 1, 2008; 294(2): G576 - G588. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Konopka, J. Tekiela, M. Iverson, C. Wells, and S. A. Duncan Junctional Adhesion Molecule-A Is Critical for the Formation of Pseudocanaliculi and Modulates E-cadherin Expression in Hepatic Cells J. Biol. Chem., September 21, 2007; 282(38): 28137 - 28148. [Abstract] [Full Text] [PDF]
|
|
