Loss of both GATA4 and GATA6 blocks cardiac myocyte differentiation and results in acardia in mice. Dev Biol 2008 May 15;317(2):614-9
Date
04/11/2008Pubmed ID
18400219Pubmed Central ID
PMC2423416DOI
10.1016/j.ydbio.2008.03.013Scopus ID
2-s2.0-43049103483 (requires institutional sign-in at Scopus site) 178 CitationsAbstract
Despite significant advances in identifying signaling molecules that induce cardiogenesis in mammals, the transcription factors that control the onset of cardiac myocyte gene expression have remained elusive. Candidates include the zinc finger transcription factors GATA binding proteins 4 and 6 (GATA4, GATA6). The individual loss of either protein in mice results in lethality prior to the onset of heart development due to defects in the extra-embryonic endoderm; however, when this extra-embryonic deficiency is circumvented using tetraploid embryo complementation, cardiac myocyte differentiation initiates normally. Here we show that these factors have redundant roles in controlling the onset of cardiac myocyte differentiation. As a consequence, Gata4(-/-)Gata6(-/-) embryos completely lack hearts, although second heart field progenitor cells are still generated. Our data support a model whereby GATA4 or GATA6 are essential for expression of the network of transcription factors that regulate the onset of cardiac myocyte gene expression during mammalian development.
Author List
Zhao R, Watt AJ, Battle MA, Li J, Bondow BJ, Duncan SAMESH terms used to index this publication - Major topics in bold
AnimalsCell Differentiation
Endoderm
GATA4 Transcription Factor
GATA6 Transcription Factor
Gene Expression Regulation, Developmental
Heart
Immunohistochemistry
In Situ Hybridization
Mice
Mice, Knockout
Models, Biological
Myocytes, Cardiac
Oligonucleotides
Reverse Transcriptase Polymerase Chain Reaction
