PMID:14614148

Citation	Katz, SG, Williams, A, Yang, J, Fujiwara, Y, Tsang, AP, Epstein, JA and Orkin, SH (2003) Endothelial lineage-mediated loss of the GATA cofactor Friend of GATA 1 impairs cardiac development. Proc. Natl. Acad. Sci. U.S.A. 100:14030-5
Abstract	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.
Links	PubMed PMC283540 Online version:10.1073/pnas.1936250100
Keywords	Animals; Carrier Proteins/genetics; Carrier Proteins/physiology; DNA-Binding Proteins/metabolism; Endothelium/embryology; Erythroid-Specific DNA-Binding Factors; Fetal Heart/abnormalities; Fetal Heart/embryology; Fetal Heart/metabolism; GATA1 Transcription Factor; Heart Defects, Congenital/embryology; Heart Defects, Congenital/genetics; Heart Valves/abnormalities; Heart Valves/embryology; Hematopoiesis/genetics; Hematopoiesis/physiology; In Situ Hybridization; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Neural Crest/embryology; Nuclear Proteins/deficiency; Nuclear Proteins/genetics; Nuclear Proteins/physiology; Transcription Factors/metabolism
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