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Muscleblind‐like 1 is a negative regulator of TGF‐β‐dependent epithelial–mesenchymal transition of atrioventricular canal endocardial cells
Author(s) -
Vajda Natalie A.,
Brimacombe Kyle R.,
LeMasters Kathryn E.,
Ladd Andrea N.
Publication year - 2009
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22155
Subject(s) - biology , regulator , endocardium , atrioventricular cushions , microbiology and biotechnology , heart development , atrioventricular canal , gene knockdown , mesoderm , mesenchyme , mesenchymal stem cell , epithelial–mesenchymal transition , atrioventricular valve , alternative splicing , transforming growth factor , embryonic stem cell , anatomy , medicine , transition (genetics) , genetics , ventricle , gene isoform , gene , heart disease
The development of the valves and septa of the heart depends on the formation and remodeling of endocardial cushions. Here, we report that the alternative splicing regulator muscleblind‐like 1 (MBNL1) exhibits a regionally restricted pattern of expression in canal region endocardium and ventricular myocardium during endocardial cushion development in chicken. Knockdown of MBNL1 in atrioventricular explants leads to a transforming growth factor β‐dependent increase in epithelial–mesenchymal transition (EMT) of endocardial cells. This reveals a novel role for MBNL1 during embryonic development, and represents the first evidence that an alternative splicing regulator is a key player in endocardial cushion development. Developmental Dynamics 238:3266–3272, 2009. © 2009 Wiley‐Liss, Inc.