Journal
DEVELOPMENTAL BIOLOGY
Volume 241, Issue 1, Pages 34-46Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/dbio.2001.0424
Keywords
endoderm; stomach; transcription factor; H+; K+-ATPase; sonic hedgehog
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P50HL061006, T32HL007873] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK052574, R01DK058529] Funding Source: NIH RePORTER
- NHLBI NIH HHS [P50 HL61006, T32-HL07873] Funding Source: Medline
- NIDDK NIH HHS [DK58529, DK 52574] Funding Source: Medline
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During mouse embryogenesis GATA-4 is expressed first in primitive endoderm and then in definitive endoderm derivatives, including glandular stomach and intestine. To explore the role of GATA-4 in specification of definitive gastric endoderm, we generated chimeric mice by introducing Gata4(-/-) ES cells into ROSA26 morulae or blastocysts. In E14.5 chimeras, Gata4(-/-) cells were represented in endoderm lining the proximal and distal stomach. These cells expressed early cytodifferentiation markers, including GATA-6 and ApoJ. However, by E18.5, only rare patches of Gata4(-/-) epithelium were evident in the distal stomach. This heterotypic epithelium had a squamous morphology and did not express markers associated with differentiation of gastric epithelial cell lineages. Sonic Hedgehog, an endoderm-derived signaling molecule normally down-regulated in the distal stomach, was overexpressed in Gata4(-/-) cells. We conclude that GATA-4-deficient cells have an intrinsic defect in their ability to differentiate. Similarities in the phenotypes of Gata4(-/-) chimeras and mice with other genetically engineered mutations that affect gut development suggest that GATA-4 may be involved in the gastric epithelial response to members of the TGF-beta superfamily. (C) 2001 Elsevier Science.
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