Maternal and zygotic Zfp57 modulate NOTCH signaling in cardiac development
Copyright policy )Maternal and zygotic Zfp57 modulate NOTCH signaling in cardiac development
Significance Abnormal heart development is a common birth defect. Genomic imprinting is absolutely essential for mammalian embryonic development. We found that loss of ZFP57, a master regulator of genomic imprinting, causes a number of heart morphogenetic defects. These cardiac defects are reminiscent of mutant phenotypes observed in the NOTCH signaling pathway, one of the most important pathways in development. Indeed, we demonstrate that NOTCH signaling is diminished without ZFP57. Furthermore, the maternal function of Zfp57 contributes to NOTCH signaling and embryonic heart development. Maternal and zygotic Zfp57 play redundant roles in genomic imprinting, NOTCH signaling, and heart development. Thus, our results provide mechanistic links among maternal effect, genomic imprinting, NOTCH signaling, and cardiac development.
- University of Chicago United States
- Academy of Military Medical Sciences China (People's Republic of)
- Icahn School of Medicine at Mount Sinai United States
- State Key Laboratory of Proteomics China (People's Republic of)
Heart Defects, Congenital, Homeodomain Proteins, Receptors, Notch, Calcium-Binding Proteins, Down-Regulation, Gene Expression Regulation, Developmental, Cell Differentiation, Heart, Embryo, Mammalian, Models, Biological, Genomic Imprinting, Mice, Animals, Newborn, Mutation, Homeobox Protein Nkx-2.5, Animals, Intercellular Signaling Peptides and Proteins, Female, Myocytes, Cardiac, Cell Proliferation
Heart Defects, Congenital, Homeodomain Proteins, Receptors, Notch, Calcium-Binding Proteins, Down-Regulation, Gene Expression Regulation, Developmental, Cell Differentiation, Heart, Embryo, Mammalian, Models, Biological, Genomic Imprinting, Mice, Animals, Newborn, Mutation, Homeobox Protein Nkx-2.5, Animals, Intercellular Signaling Peptides and Proteins, Female, Myocytes, Cardiac, Cell Proliferation
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