The inner nuclear membrane protein Emerin regulates beta-cateninactivity by restricting its accumulation in the nucleus

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  2. Dr Katarzyna Tilgner
  3. Professor Christopher Hutchison
Author(s)Markiewicz E, Tilgner K, Barker N, van de Wetering M, Clevers H, Dorobek M, Hausmanowa-Petrusewicz I, Ramaekers FCS, Broers JLV, Blankesteijn WM, Salpingidou G, Wilson RG, Ellis JA, Hutchison CJ
Publication type Article
JournalEMBO Journal
Year2007
Volume25
Issue14
Pages3275-3285
ISSN (print)0261-4189
ISSN (electronic)1460-2075
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Emerin is a type II inner nuclear membrane (INM) protein of unknown function. Emerin function is likely to be important because, when it is mutated, emerin promotes both skeletal muscle and heart defects. Here we show that one function of Emerin is to regulate the flux of -catenin, an important transcription coactivator, into the nucleus. Emerin interacts with -catenin through a conserved adenomatous polyposis coli (APC)-like domain. When GFP-emerin is expressed in HEK293 cells, -catenin is restricted to the cytoplasm and -catenin activity is inhibited. In contrast, expression of an emerin mutant, lacking its APC-like domain (GFP-emerin), dominantly stimulates -catenin activity and increases nuclear accumulation of -catenin. Human fibroblasts that are null for emerin have an autostimulatory growth phenotype. This unusual growth phenotype arises through enhanced nuclear accumulation and activity of -catenin and can be replicated in wild-type fibroblasts by transfection with constitutively active -catenin. Our results support recent findings that suggest that INM proteins can influence signalling pathways by restricting access of transcription coactivators to the nucleus.
PublisherNature Publishing Group
URLhttp://dx.doi.org/10.1038/sj.emboj.7601230
DOI10.1038/sj.emboj.7601230
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