Willin and Par3 cooperatively regulate epithelial apical constriction through aPKC-mediated ROCK phosphorylation

Takashi Ishiuchi, Masatoshi Takeichi

Research output: Contribution to journalArticlepeer-review

78 Citations (Scopus)

Abstract

Apical-domain constriction is important for regulating epithelial morphogenesis. Epithelial cells are connected by apical junctional complexes (AJCs) that are lined with circumferential actomyosin cables. The contractility of these cables is regulated by Rho-associated kinases (ROCKs). Here, we report that Willin (a FERM-domain protein) and Par3 (a polarity-regulating protein) cooperatively regulate ROCK-dependent apical constriction. We found that Willin recruits aPKC and Par6 to the AJCs, independently of Par3. Simultaneous depletion of Willin and Par3 completely removed aPKC and Par6 from the AJCs and induced apical constriction. Induced constriction was through upregulation of the level of AJC-associated ROCKs, which was due to loss of aPKC. Our results indicate that aPKC phosphorylates ROCK and suppresses its junctional localization, thereby allowing cells to retain normally shaped apical domains. Thus, we have uncovered a Willin/Par3aPKCROCK pathway that controls epithelial apical morphology.

Original languageEnglish
Pages (from-to)860-866
Number of pages7
JournalNature Cell Biology
Volume13
Issue number7
DOIs
Publication statusPublished - Jul 1 2011
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Cell Biology

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