| Literature DB >> 11297508 |
J D Crispino1, M B Lodish, B L Thurberg, S H Litovsky, T Collins, J D Molkentin, S H Orkin.
Abstract
GATA-family transcription factors are critical to the development of diverse tissues. In particular, GATA-4 has been implicated in formation of the vertebrate heart. As the mouse Gata-4 knock-out is early embryonic lethal because of a defect in ventral morphogenesis, the in vivo function of this factor in heart development remains unresolved. To search for a requirement for Gata4 in heart development, we created mice harboring a single amino acid replacement in GATA-4 that impairs its physical interaction with its presumptive cardiac cofactor FOG-2. Gata4(ki/ki) mice die just after embryonic day (E) 12.5 exhibiting features in common with Fog2(-/-) embryos as well as additional semilunar cardiac valve defects and a double-outlet right ventricle. These findings establish an intrinsic requirement for GATA-4 in heart development. We also infer that GATA-4 function is dependent on interaction with FOG-2 and, very likely, an additional FOG protein for distinct aspects of heart formation.Entities:
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Year: 2001 PMID： 11297508 PMCID： PMC312667 DOI： 10.1101/gad.875201
Source DB: PubMed Journal: Genes Dev ISSN： 0890-9369 Impact factor: 11.361