Transcription regulator that plays a central role in heart morphogenesis and development of coronary vessels from epicardium, by regulating genes that are essential during cardiogenesis. Essential cofactor that acts via the formation of a heterodimer with transcription factors of the GATA family GATA4, GATA5 and GATA6. Such heterodimer can both activate or repress transcriptional activity, depending on the cell and promoter context. Also required in gonadal differentiation, possibly be regulating expression of SRY. Probably acts a corepressor of NR2F2. Interacts with the N-terminal zinc-finger of GATA4, GATA5 and probably GATA6. Interacts with retinoid nuclear receptor RXRA when ligand bound. Interacts with corepressor CTBP2; this interaction is however not essential for corepressor activity. Interacts with NR2F2 and NR2F6. Interacts with ATOH8; mediates indirect interaction with GATA4. Expressed in heart, brain and testis. Weakly expressed in lung and liver. First expressed at approximately E8.5 in the developing ventral heart tube and septum transversum. Cardiac expression persists throughout the remainder of embryonic development in the atria as well as in all layers of the ventricles (endocardium, myocardium, and pericardium). Expressed in the neuroepithelium of the developing midbrain and hindbrain from 11.5 dpc and increased in intensity between 12 dpc and 16.5 dpc. Also expressed in the urogenital ridge beginning at 11.5 dpc and subsequently localized to the gonads by 16.5 dpc. Colocalizes with GATA4 GATA5 and GATA6 in the developing heart, GATA3 in the brain, and GATA4 in the gonads. The CCHC FOG-type zinc fingers 1, 2, 3 and 5 directly bind to GATA-type zinc fingers. The Tyr residue adjacent to the last Cys of the CCHC FOG-type zinc finger is probably essential for the interaction with GATA-type zinc fingers. Sumoylation reduces transcriptional repression activity. Mice die of congestive heart failure at 13 dpc with a syndrome of tricuspid atresia that includes an absent tricuspid valve, a large atrial and ventricular spetal defects, an elongated left ventricular outflow tract, rightward displacement of the aortic valve and pulmonic stenosis. These mice also display hypoplasia of the compact zone of the left ventricle. Splicing donor site between exon 3 and 4 is not canonical. Belongs to the FOG (Friend of GATA) family.