2004
DOI: 10.1073/pnas.0400752101
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Abstract: The role of GATA4 during the earliest stages of cardiogenesis has not been defined because Gata4 knockout embryos suffer an early developmental arrest caused by deficiencies in extraembryonic visceral endoderm function. We have used tetraploid embryo complementation to rescue these defects and generated clonal embryonic day 9.5 Gata4 ؊/؊ embryos directly from embryonic stem cells. GATA4-null embryos display heart defects characterized by disrupted looping morphogenesis, septation, and a hypoplastic ventricular… Show more

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Cited by 311 publications
(321 citation statements)
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“…E8.5 Gata4 -/-mouse embryos exhibit severe defects in ventral morphogenesis (Kuo et al, 1997;Molkentin et al, 1997), which can be abrogated by wild type endoderm (Narita et al, 1997b;Bielinska et al, 1999;Watt et al, 2004). This indicates that expression of GATA-4 in early endoderm, presumably visceral endoderm, is required for ventral morphogenesis and foregut invagination.…”
Section: Resultsmentioning
confidence: 99%
See 1 more Smart Citation
“…E8.5 Gata4 -/-mouse embryos exhibit severe defects in ventral morphogenesis (Kuo et al, 1997;Molkentin et al, 1997), which can be abrogated by wild type endoderm (Narita et al, 1997b;Bielinska et al, 1999;Watt et al, 2004). This indicates that expression of GATA-4 in early endoderm, presumably visceral endoderm, is required for ventral morphogenesis and foregut invagination.…”
Section: Resultsmentioning
confidence: 99%
“…Gata4 null mice die by E9.5, so insights into gut morphogenesis cannot be ascertained from these animals (Kuo et al, 1997;Molkentin et al, 1997;Narita et al, 1997b;Watt et al, 2004). In chimeric mice, Gata4 -/-cells can contribute to invaginating foregut epithelium, but these cells exhibit deregulated gene expression and impaired epithelial-mesenchymal signaling (Jacobsen et al, 2002).…”
Section: Introductionmentioning
confidence: 99%
“…2I,J), and GATA-4 transcription factor (Fig. 2G,H), all of which are essential for maintaining a differentiated phenotype in cardiomyocyte lineage (Watt et al, 2004;Wang et al, 2006).…”
Section: Foxm1 ؊/؊ Embryonic Hearts Exhibited Ventricular Hypoplasiamentioning
confidence: 99%
“…Disruption of this transcriptional network results in a variety of human diseases including congenital heart disease, dilated cardiomyopathy, and cardiac hypertrophy (Frey and Olson, 2003;Olson, 2004;Clark et al, 2006). Central to the regulation of these developmental processes are the cardiac transcription factors GATA4 (Watt et al, 2004), NKX2.5 (Cripps and Olson, 2002), Hand (McFadden et al, 2005), nuclear factors of activated T-cell (NFAT) c3 and c4 (Molkentin, 2000;Graef et al, 2001;Bushdid et al, 2003), Foxp4 and FOG2 (Svensson et al, 2000;Lin et al, 2004), and T-box transcription factors TBX1 and TBX5 (Plageman and Yutzey, 2005), all of which have been shown to regulate cardiomyocyte proliferation, cardiacspecific gene expression, and proper patterning of the developing heart.…”
Section: Introductionmentioning
confidence: 99%
“…For example, transcription factors GATA4, MEF2A, NKX2.5 and TBX5 each have critical roles in vertebrate heart development, maturation and function, working in concert with developmental signaling pathways, environmental influences, and chromatin regulatory machinery. Knockout of any of these genes in mice leads to defects in cardiogenesis and embryonic or early postnatal lethality (1)(2)(3)(4). It is challenging to define a precise regulatory hierarchy, as these genes regulate the expression of each other (and themselves), and their encoded proteins interact functionally in complexes that somehow together regulate distinct genesets important for diverse developmental programs, such as chamber growth, septation, valve formation, and outflow tract development.…”
Section: Background and Significancementioning
confidence: 99%