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EMBO reports 8, 2, 158–164 (2007)
doi:10.1038/sj.embor.7400890
AOP Published online: 19 January 2007
PATJ regulates directional migration of mammalian epithelial cells
Kunyoo Shin1, Qian Wang1 & Ben Margolis1, 2
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1 Department of Biological Chemistry, University of Michigan Medical School, Room 1528, BSRB, 109 Zina Pitcher Place, Ann Arbor, Michigan 48109-2200, USA
2 Department of Internal Medicine, University of Michigan Medical School, Room 1528, BSRB, 109 Zina Pitcher Place, Ann Arbor, Michigan 48109-2200, USA
To whom correspondence should be addressed
Ben Margolis Tel: +1 734 764 3567; Fax: +1 734 615 4356; E-mail: bmargoli@umich.edu
Received 31 July 2006; Accepted 23 November 2006; Published online 19 January 2007.
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Abstract
Directional migration is important in wound healing by epithelial cells. Recent studies have shown that polarity proteins such as mammalian Partitioning-defective 6 (Par6), atypical protein kinase C (aPKC) and mammalian Discs large 1 (Dlg1) are crucial not only for epithelial apico-basal polarity, but also for directional movement. Here, we show that the protein associated with Lin seven 1 (PALS1)-associated tight junction protein (PATJ), another evolutionarily conserved polarity protein, is also required for directional migration by using a wound-induced migration assay. In addition, we found that aPKC and Par3 localize to the leading edge during migration of epithelia and that PATJ regulates their localization. Furthermore, our results show that microtubule-organizing centre orientation is disrupted in PATJ RNA interference (RNAi) MDCKII (Madin–Darby canine kidney II) cells during migration. Together, our data indicate that PATJ controls directional migration by regulating the localization of aPKC and Par3 to the leading edge. The migration defect in PATJ RNAi cells seems to be due to the disorganization of the microtubule network induced by mislocalization of polarity proteins.
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