Epithelial junctions maintain tissue architecture by directing planar spindle orientation

Overview
TitleEpithelial junctions maintain tissue architecture by directing planar spindle orientation
AuthorsNakajima Y, Meyer EJ, Kroesen A, McKinney SA, Gibson MC
TypeJournal Article
Journal NameNature
Volume500
Issue7462
Year2013
Page(s)359-62
CitationNakajima Y, Meyer EJ, Kroesen A, McKinney SA, Gibson MC. Epithelial junctions maintain tissue architecture by directing planar spindle orientation. Nature. 2013 Aug 15; 500(7462):359-62.

Abstract

During epithelial cell proliferation, planar alignment of the mitotic spindle coordinates the local process of symmetric cell cleavage with the global maintenance of polarized tissue architecture. Although the disruption of planar spindle alignment is proposed to cause epithelial to mesenchymal transition and cancer, the in vivo mechanisms regulating mitotic spindle orientation remain elusive. Here we demonstrate that the actomyosin cortex and the junction-localized neoplastic tumour suppressors Scribbled and Discs large 1 have essential roles in planar spindle alignment and thus the control of epithelial integrity in the Drosophila imaginal disc. We show that defective alignment of the mitotic spindle correlates with cell delamination and apoptotic death, and that blocking the death of misaligned cells is sufficient to drive the formation of basally localized tumour-like masses. These findings indicate a key role for junction-mediated spindle alignment in the maintenance of epithelial integrity, and also reveal a previously unknown cell-death-mediated tumour-suppressor function inherent in the polarized architecture of epithelia.

Properties
Additional details for this publication include:
Property NameValue
Publication ModelPrint-Electronic
ISSN1476-4687
eISSN1476-4687
Publication Date2013 Aug 15
Journal AbbreviationNature
DOI10.1038/nature12335
Elocation10.1038/nature12335
LanguageEnglish
Language Abbreng
Publication TypeJournal Article
Journal CountryEngland
Publication TypeResearch Support, Non-U.S. Gov't
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DatabaseAccession
PMID: PMID:23873041