Localization of transcription factor GATA-4 to regions of the mouse embryo involved in cardiac development

Heikinheimo, Markku; Scandrett, John M.; Wilson, David B.

doi:10.1006/dbio.1994.1206

Cited by 277 publications

(166 citation statements)

References 46 publications

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“…Thus, these experiments were consistent with the hypothesis that the major GATA-4-binding activity present in cardiac extracts is derived from the cardiac myocyte population. In addition, they are in agreement with previous studies that have suggested a lack of GATA-4 expression in skeletal myocytes (4,23,75).…”

Section: Resultssupporting

confidence: 93%

“…7D and E, arrows), which include precardiac mesoderm and liver precursors in the septum transversum, were found to express GATA-4 mRNA but not cTnC mRNA. These results and earlier studies (23) .5-day p.c. embryo hybridized to a GATA-4 antisense probe.…”

Section: Resultssupporting

confidence: 92%

“…Several lines of evidence now suggest that GATA-4 may play an important role in cardiac muscle development. GATA-4 is expressed early during cardiac myogenesis in the mouse, and its expression is restricted to the developing heart and precardiac mesoderm during early murine development (4,23). GATA-4-binding sites are present in the transcriptional regulatory regions of multiple cardiac genes (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…In the mouse, the GATA-4 gene is first expressed in the coelomic epithelial cells of the primitive streak embryo at postcoital (p.c.) day 7 (23). GATA-4 mRNA is clearly detectable within the primordial heart tube at p.c.…”

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confidence: 97%

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The GATA-4 transcription factor transactivates the cardiac muscle-specific troponin C promoter-enhancer in nonmuscle cells.

Ip¹,

Wilson²,

Heikinheimo³

et al. 1994

Mol. Cell. Biol.

171

104

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The unique contractile phenotype of cardiac myocytes is determined by the expression of a set of cardiac muscle-specific genes. By analogy to other mammalian developmental systems, it is likely that the coordinate expression of cardiac genes is controlled by lineage-specific transcription factors that interact with promoter and enhancer elements in the transcriptional regulatory regions of these genes. Although previous reports have identified several cardiac muscle-specific transcriptional elements, relatively little is known about the lineage-specific transcription factors that regulate these elements. In this report, we demonstrate that the slow/cardiac muscle-specific troponin C (cTnC) enhancer contains a specific binding site for the lineagerestricted zinc finger transcription factor GATA-4. This (7, 10,27,35,48,65,81). Therefore, an understanding of muscle cell development must at some level be based upon elucidating the molecular mechanisms that control lineage-specific gene expression during myogenesis.The recent identification and characterization of the basic helix-loop-helix myogenic transcription factors, including MyoD, myogenin, Myf-5, and MRF-4/herculin/Myf-6, as well as the MEF-2 family of transcription factors has added significantly to our understanding of skeletal myogenesis (8, 9,12,15,18,40,41,43,58,59,76,80). These factors bind to and regulate the expression of many skeletal muscle-specific genes (47,48,64,70). In contrast, relatively little is currently understood about the molecular mechanisms that control cardiac muscle-specific gene expression during mammalian development. Despite the fact that overlapping sets of genes are expressed in the heart and skeletal muscle, several lines of evidence suggest that distinct transcriptional programs may regulate these processes. For example, basic helix-loop-helix myogenic transcription factors are not expressed in developing heart or precardiac mesoderm (49,63,64), and mice contain-* Corresponding author. Mailing address:

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Section: Resultssupporting

confidence: 93%

Section: Resultssupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 97%

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The GATA-4 transcription factor transactivates the cardiac muscle-specific troponin C promoter-enhancer in nonmuscle cells.

Ip¹,

Wilson²,

Heikinheimo³

et al. 1994

Mol. Cell. Biol.

171

104

View full text Add to dashboard Cite

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“…Frozen sections (10 m) were fixed with 4% paraformaldehyde and subjected to in situ hybridization as described (Heikinheimo et al, 1994). Sections were incubated with 10 6 cpm of [ 33 P]-labeled antisense riboprobe prepared using the following linearized plasmid templates and RNA polymerases: (1) GATA-4, BamHI digested pBluescript SK phagemid G14a (Arceci et al, 1993), T7 polymerase; (2) Shh, HindIII-digested pBluescript SK plasmid containing the cDNA, T3 polymerase (Bitgood and McMahon, 1995); (3) FGF-10, 584 nucleotide cDNA fragment, BamHI digested pBluescript KS II, T3 polymerase (Pauley et al, 2003).…”

Section: In Situ Hybridizationmentioning

confidence: 99%

GATA‐4:FOG interactions regulate gastric epithelial development in the mouse

Jacobsen¹,

Mannisto²,

Porter-Tinge³

et al. 2005

Developmental Dynamics

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Transcription factor GATA-4 is a key participant in cytodifferentiation of the mouse hindstomach. Here we show that GATA-4 cooperates with a Friend-of-GATA (FOG) cofactor to direct gene expression in this segment of gut. Immunohistochemical staining revealed that GATA-4 and FOG-1 are co-expressed in hindstomach epithelial cells from embryonic days (E) 11.5 to 18.5. The other member of the mammalian FOG family, FOG-2, was not detected in gastric epithelium. To show that GATA-4:FOG interactions influence stomach development, we analyzed Gata4 ki/ki mice, which express a mutant GATA-4 that cannot bind FOG cofactors. Sonic Hedgehog, an endoderm-derived signaling molecule normally down-regulated in the distal stomach, was over-expressed in hindstomach epithelium of E11.5 Gata4 ki/ki mice, and there was a concomitant decrease in fibroblast growth factor-10 in adjacent mesenchyme. We conclude that functional interaction between GATA-4 and a member of the FOG family, presumably FOG-1, is required for proper epithelial-mesenchymal signaling in the developing stomach. Developmental Dynamics 234:355-362, 2005.

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GATA4 haploinsufficiency in patients with interstitial deletion of chromosome region 8p23.1 and congenital heart disease

et al. 1999

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Previous studies have shown that patients with deletion of distal human chromosome arm 8p may have congenital heart disease and other physical anomalies. The gene encoding GATA-4, a zinc finger transcription factor implicated in cardiac gene expression and development, localizes to chromosome region 8p23.1. To examine whether GATA-4 deficiency is present in patients with monosomy of 8p23.1 with congenital heart disease, we performed fluorescence in situ hybridization (FISH) with a GATA4 probe on cells from a series of patients with interstitial deletion of 8p23.1. Four individuals with del(8)(p23.1) and congenital heart disease were found to be haploinsufficient at the GATA4 locus by FISH. The GATA4 gene was not deleted in a fifth patient with del(8)(p23.1) who lacked cardiac anomalies. FISH analysis on cells from 48 individuals with congenital heart disease and normal karyotypes failed to detect any submicroscopic deletions at the GATA4 locus. We conclude that haploinsufficiency at the GATA4 locus is often seen in patients with del(8)(p23.1) and congenital heart disease. Based on these findings and recent studies showing that haploinsufficiency for other cardiac transcription factor genes (e.g., TBX5, NKX2-5) causes congenital heart disease, we postulate that GATA-4 deficiency may contribute to the phenotype of patients with monosomy of 8p23.1.

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Localization of transcription factor GATA-4 to regions of the mouse embryo involved in cardiac development

Cited by 277 publications

References 46 publications

The GATA-4 transcription factor transactivates the cardiac muscle-specific troponin C promoter-enhancer in nonmuscle cells.

The GATA-4 transcription factor transactivates the cardiac muscle-specific troponin C promoter-enhancer in nonmuscle cells.

GATA‐4:FOG interactions regulate gastric epithelial development in the mouse

GATA4 haploinsufficiency in patients with interstitial deletion of chromosome region 8p23.1 and congenital heart disease

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