QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online 15 July 2008
doi: 10.1242/jcs.024109

This Article Figures Only Full Text Full Text (PDF) Supplementary Material All Versions of this Article: jcs.024109v1 121/15/2481    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kishikawa, M. Articles by Ohno, S. Search for Related Content PubMed PubMed Citation Articles by Kishikawa, M. Articles by Ohno, S. Social Bookmarking                         What's this?

aPKC enables development of zonula adherens by antagonizing centripetal contraction of the circumferential actomyosin cables

Department of Molecular Biology, Yokohama City University Graduate School of Medical Science, 3-9 Fuku-ura, Kanazawa-ku, Yokohama, 236-0004, Japan

^* Author for correspondence (e-mail: abell{at}med.yokohama-cu.ac.jp)

Accepted 12 May 2008

Atypical protein kinase C (aPKC) generally plays crucial roles in the establishment of cell polarity in various biological contexts. In mammalian epithelial cells, aPKC essentially works towards the transition of primordial spot-like adherens junctions (AJs) into continuous belt-like AJs, also called zonula adherens, lined with perijunctional actin belts. To reveal the mechanism underlying this aPKC function, we investigated the functional relationship between aPKC and myosin II, the essential role of which in epithelial-junction development was recently demonstrated. Despite its deleterious effects on junction formation, overexpression of a dominant-negative mutant of aPKC (aPKC kn) did not interfere with the initial phase of myosin-II activation triggered by the formation of Ca²⁺-switch-induced cell-cell contacts. Furthermore, cells overexpressing aPKC kn exhibited myosin-II-dependent asymmetric organization of F-actin along the apicobasal axis, suggesting that aPKC contributes to junction development without affecting the centripetal contraction of the circumferential actomyosin cables. Time-lapse analyses using GFP-actin directly revealed that the circumferential actomyosin cables were centrifugally expanded and developed into perijunctional actin belts during epithelial polarization, and that aPKC kn specifically compromised this process. Taken together, we conclude that aPKC is required for antagonizing the myosin-II-driven centripetal contraction of the circumferential actin cables, thereby efficiently coupling the myosin-II activity with junction development and cell polarization. The present results provide novel insights into not only the site of action of aPKC kinase activity but also the role of actomyosin contraction in epithelial polarization.

Key words: PAR, aPKC, Actin dynamics, Adherens junction, Epithelial cells, Polarity

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				M. K. Nyholm, S. Abdelilah-Seyfried, and Y. Grinblat A novel genetic mechanism regulates dorsolateral hinge-point formation during zebrafish cranial neurulation J. Cell Sci., June 15, 2009; 122(12): 2137 - 2148. [Abstract] [Full Text] [PDF]