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PMID: 15689382 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Characterization of Nfatc1 regulation identifies an enhancer required for gene expression that is specific to pro-valve endocardial cells in the developing heart.

Development (Cambridge, England) ·Vol. 132 ·No. 5 ·2005-03-00 ·Pages 1137-46

Zhou B, Wu B, Tompkins KL, Boyer KL, Grindley JC, Baldwin HS

Abstract

Nfatc1 is an endocardial transcription factor required for development of cardiac valves. Herein, we describe identification and characterization of a tissue-specific enhancer in the first intron of murine Nfatc1 that activates a heterogenic promoter and directs gene expression in a subpopulation of endocardial cells of the developing heart: the pro-valve endocardial cells. This enhancer activity begins on embryonic day (E) 8.5 in endocardial cells at the ventricular end of the atrioventricular canal, intensifies and extends from E9.5 to E11.5 in endocardium along the atrioventricular canal and outflow tract. By E12.5, the enhancer activity is accentuated in endocardial cells of forming valves. Sequential deletion analysis identified that a 250 bp DNA fragment at the 3' end of the intron 1 is required for endocardial-specific activity. This region contains two short conserved sequences hosting a cluster of binding sites for transcription factors, including Nfat and Hox proteins. Electrophoresis mobility shift and chromatin immunoprecipitation assays demonstrated binding of Nfatc1 to the Nfat sites, and inactivation of Nfatc1 downregulated the enhancer activity in pro-valve endocardial cells. By contrast, mutation of the Hox site abolished its specificity, allowing gene expression in non pro-valve endocardium and extracardiac vasculature. Thus, autoregulation of Nfatc1 is required for maintaining high Nfatc1 expression in pro-valve endocardial cells, while suppression through the Hox site prevents its expression outside pro-valve endocardial cells during valve development. Our data demonstrate the first autonomous cell-specific enhancer for pro-valve endocardial cells and delineate a unique transcriptional mechanism that regulates endocardial Nfatc1 expression within developing cardiac valves.

MeSH Terms
Animals Binding Sites Cells, Cultured Chromatin Immunoprecipitation DNA/metabolism DNA-Binding Proteins/genetics,physiology Endocardium/embryology Enhancer Elements, Genetic Gene Deletion Gene Expression Regulation Gene Expression Regulation, Developmental Heart/embryology Heart Valves/embryology Homeodomain Proteins/metabolism Introns Mice Mice, Transgenic Models, Genetic Mutation Myocardium/metabolism NFATC Transcription Factors Nuclear Proteins/genetics,physiology Promoter Regions, Genetic RNA, Messenger/metabolism Time Factors Transcription Factors/genetics,physiology Transcription, Genetic Transgenes beta-Galactosidase/metabolism
Chemicals
DNA-Binding Proteins Homeodomain Proteins NFATC Transcription Factors Nfatc1 protein, mouse Nuclear Proteins RNA, Messenger Transcription Factors DNA beta-Galactosidase
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Zhou Bin
Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. bin.zhou@vanderbilt.edu
Wu Bingruo
Tompkins Kevin L
Boyer Kathleen L
Grindley Justin C
Baldwin H Scott
Article Info
Journal
Development (Cambridge, England)
Abbr.
Development
ISSN
0950-1991
Published
2005-03-00
Epub
2005-00-02
Pages
1137-46
Language
English
Region
England
NLM ID
8701744
Subset
IM
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