Document Detail


Endothelial lineage-mediated loss of the GATA cofactor Friend of GATA 1 impairs cardiac development.
MedLine Citation:
PMID:  14614148     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
GATA transcription factors, together with Friend of GATA (FOG) cofactors, are required for the differentiation of diverse cell types. Multiple aspects of hematopoiesis are controlled by the interaction of FOG-1 with the GATA-1/2/3 subfamily. Likewise, FOG-2 is coexpressed with the GATA-4/5/6 subfamily at other sites, including the heart and gonads. FOG-2 and GATA-4 are required for cardiac development. Through transgenic rescue of hematopoietic defects of FOG-1-/- embryos we define an unsuspected role for FOG-1 in heart development. In particular, rescued FOG-1-/- mice die at embryonic day (E) 14.5 with cardiac defects that include double outlet right ventricle and a common atrioventricular valve. Using conditional inactivation of Fog-1 we assign the cell of origin in which FOG-1 function is required. Neural crest cells migrate properly into FOG-1-/- hearts and mice with FOG-1 conditionally excised from neural crest derivatives fail to develop cardiac abnormalities. In contrast, conditional inactivation of FOG-1 in endothelial-derived tissues by means of Tie-2-expressed Cre recapitulates the rescue-knockout defects. These findings establish a nonredundant requirement for FOG-1 in the outlet tract and atrioventricular valves of the heart that depend on expression in endothelial-derived tissue and presumably reflect cooperation with the GATA-4/5/6 subfamily.
Authors:
Samuel G Katz; Aimee Williams; Jifu Yang; Yuko Fujiwara; Alice P Tsang; Jonathan A Epstein; Stuart H Orkin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2003-11-12
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  100     ISSN:  0027-8424     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2003 Nov 
Date Detail:
Created Date:  2003-12-03     Completed Date:  2004-02-02     Revised Date:  2013-04-18    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  14030-5     Citation Subset:  IM    
Affiliation:
Division of Hematology/Oncology, Children's Hospital and Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Carrier Proteins / genetics,  physiology
DNA-Binding Proteins / metabolism
Endothelium / embryology
Erythroid-Specific DNA-Binding Factors
Fetal Heart / abnormalities,  embryology*,  metabolism
GATA1 Transcription Factor
Heart Defects, Congenital / embryology,  genetics
Heart Valves / abnormalities,  embryology
Hematopoiesis / genetics,  physiology
In Situ Hybridization
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Neural Crest / embryology
Nuclear Proteins / deficiency*,  genetics,  physiology
Transcription Factors / metabolism
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/DNA-Binding Proteins; 0/Erythroid-Specific DNA-Binding Factors; 0/GATA1 Transcription Factor; 0/Gata1 protein, mouse; 0/Nuclear Proteins; 0/Transcription Factors; 0/Zfpm1 protein, mouse
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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