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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Ng, Sheau-fang Yang, Guan Liu, Lizhi Takikawa, Sachiko Moskowitz, Ivan P. Xiao, Lijuan Ray, Chelsea Yang, Xiao Cullen, Dana E. Cai, Chen-leng Bell, Fong T. Li, Xiajun Shamis, Yulia |
| Description | Author Affiliation: Shamis Y ( Department of Developmental and Regenerative Biology, Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029); Cullen DE ( Department of Developmental and Regenerative Biology.); Liu L ( Department of Developmental and Regenerative Biology.); Yang G ( State Key Laboratory of Proteomics, Genetic Laboratory of Development and Diseases, Institute of Biotechnology, Beijing 100071, China); Ng SF ( Department of Developmental and Regenerative Biology.); Xiao L ( Department of Developmental and Regenerative Biology.); Bell FT ( Department of Developmental and Regenerative Biology.); Ray C ( Department of Developmental and Regenerative Biology.); Takikawa S ( Department of Developmental and Regenerative Biology.); Moskowitz IP ( Departments of Pediatrics, Pathology, and Human Genetics, University of Chicago, Chicago, IL 60637.); Cai CL ( Department of Developmental and Regenerative Biology.); Yang X ( State Key Laboratory of Proteomics, Genetic Laboratory of Development and Diseases, Institute of Biotechnology, Beijing 100071, China); Li X ( Department of Developmental and Regenerative Biology, Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029); |
| Abstract | Zfp57 is a maternal-zygotic effect gene that maintains genomic imprinting. Here we report that Zfp57 mutants exhibited a variety of cardiac defects including atrial septal defect (ASD), ventricular septal defect (VSD), thin myocardium, and reduced trabeculation. Zfp57 maternal-zygotic mutant embryos displayed more severe phenotypes with higher penetrance than the zygotic ones. Cardiac progenitor cells exhibited proliferation and differentiation defects in Zfp57 mutants. ZFP57 is a master regulator of genomic imprinting, so the DNA methylation imprint was lost in embryonic heart without ZFP57. Interestingly, the presence of imprinted DLK1, a target of ZFP57, correlated with NOTCH1 activation in cardiac cells. These results suggest that ZFP57 may modulate NOTCH signaling during cardiac development. Indeed, loss of ZFP57 caused loss of NOTCH1 activation in embryonic heart with more severe loss observed in the maternal-zygotic mutant. Maternal and zygotic functions of Zfp57 appear to play redundant roles in NOTCH1 activation and cardiomyocyte differentiation. This serves as an example of a maternal effect that can influence mammalian organ development. It also links genomic imprinting to NOTCH signaling and particular developmental functions. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 16 |
| Volume Number | 112 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2015-04-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Heart Embryology Receptors, Notch Metabolism Repressor Proteins Signal Transduction Zygote Animals Animals, Newborn Cell Differentiation Cell Proliferation Down-Regulation Embryo, Mammalian Gene Expression Regulation, Developmental Genomic Imprinting Heart Defects, Congenital Homeodomain Proteins Intercellular Signaling Peptides And Proteins Mice Models, Biological Mutation Myocytes, Cardiac Pathology Deficiency Genetics Stem Cells Cytology Transcription Factors Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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