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The POF1B candidate genefor premature ovarian Failure regulates epithelial polarity (Articolo in rivista)

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The POF1B candidate genefor premature ovarian Failure regulates epithelial polarity (Articolo in rivista) (literal)

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Padovano V1, Lucibello I1, Alari V1, Dallamina P2, Crespi A1, Ferrari I1, Recagni M1, Lattuada D1, Righi M1,3, Toniolo D4, Villa A2, Pietrini G1,3 (2011)
The POF1B candidate genefor premature ovarian Failure regulates epithelial polarity
in Journal of cell science
(literal)

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Padovano V1, Lucibello I1, Alari V1, Dallamina P2, Crespi A1, Ferrari I1, Recagni M1, Lattuada D1, Righi M1,3, Toniolo D4, Villa A2, Pietrini G1,3 (literal)

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1Department of Pharmacology, Medical School, Universita` degli Studi di Milano, 20129 Milan, Italy 2Consorzio MIA, Universita` Milano-Bicocca, 20052 Monza, Italy 3CNR- Institute of Neuroscience, 20129 Milan, Italy 4Division of Genetics and Cell Biology, San Raffaele Scientific Institute, 20132 Milan, Italy (literal)

Titolo

The POF1B candidate genefor premature ovarian Failure regulates epithelial polarity (literal)

Abstract

POF1B is a candidate gene for premature ovarian failure (POF); it is mainly expressed in polarised epithelial tissues, but its function in these tissues and the relationship with the disorder are unknown. Here we show colocalisation of POF1B with markers of both adherens and tight junctions in human jejunum. The tight junction localisation was maintained by the human POF1B stably expressed in the MDCK polarised epithelial cell line, whereas it was lost by the POF1B R329Q variant associated with POF. Localisation of apico-basal polarity markers and ultrastructure of the tight junctions were maintained in cells expressing the mutant. However, tight junction assembly was altered, cells were dysmorphic and the monolayer organisation was also altered in three-dimensional culture systems. Moreover, cells expressing the POF1B R329Q variant showed defects in ciliogenesis and cystogenesis as a result of misorientation of primary cilia and mitotic division. All of these defects were explained by interference of the mutant with the content and organisation of F-actin at the junctions. A role for POF1B in the regulation of the actin cytoskeleton was further verified by shRNA silencing of the endogenous protein in human intestinal Caco-2 cells. Taken together, these data indicate that localisation of POF1B to tight junctions has a key role in the organisation of epithelial monolayers by regulating the actin cytoskeleton. © 2011. Published by The Company of Biologists Ltd. (literal)

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