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    
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.
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    
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
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, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Neural Crest / embryology
Nuclear Proteins / deficiency*,  genetics,  physiology
Transcription Factors / metabolism
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

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