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Busche, S.* ; Kremmer, E. ; Posern, G.*

E-cadherin regulates MAL-SRF-mediated transcription in epithelial cells.

J. Cell Sci. 123, 2803-2809 (2010)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Epithelial junctions are dynamically and functionally linked to the actin cytoskeleton, and their disassembly is a key event during physiological and pathological processes. We recently showed that epithelial disintegration facilitates transcriptional activation via Rac, G-actin, MAL (also known as MRTF) and serum response factor (SRF). Here, we investigate which specific component of the epithelial junction is essential for this MAL-SRF-mediated transcription. The Ca(2+)-dependent dissociation of polarised epithelial cells depleted of ZO proteins - which form adherens junctions (AJs) but completely lack tight junctions (TJs) - fully activated SRF. By contrast, AGS gastric adenocarcinoma epithelial cells, which form TJs but are deficient in E-cadherin, and therefore also in AJs, failed to activate SRF. The introduction of wild-type E-cadherin in AGS cells restored AJ formation and MAL-SRF inducibility. To gain further insight into the membrane-proximal signalling, AGS cells were stably transfected with E-cadherin-alpha-catenin fusions. Despite restored formation of cell-cell contacts containing the nectin-afadin complex and p120-catenin, these cells did not activate SRF upon junction dissociation, suggesting that signal transmission depends on the C-terminal tail of E-cadherin. We conclude that the dissociation of intercellular E-cadherin interactions from AJs, and signals originating from the C-terminal region covering the beta-catenin-binding site of E-cadherin, are essential for transcriptional activation via Rac, MAL and SRF, whereas TJs are not involved.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Adherens junctions; Tight junctions; Gene expression
ISSN (print) / ISBN 0021-9533
e-ISSN 1477-9137
Zeitschrift Journal of Cell Science
Quellenangaben Band: 123, Heft: 16, Seiten: 2803-2809 Artikelnummer: , Supplement: ,
Verlag Company of Biologists
Verlagsort Cambridge
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Immunology (IMI)