Shamis Yulia, Cullen Dana E, Liu Lizhi, Yang Guan, Ng Sheau-Fang, Xiao Lijuan, Bell Fong T, Ray Chelsea, Takikawa Sachiko, Moskowitz Ivan P, Cai Chen-Leng, Yang Xiao, Li Xiajun
Department of Developmental and Regenerative Biology, Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029;
Department of Developmental and Regenerative Biology.
Proc Natl Acad Sci U S A. 2015 Apr 21;112(16):E2020-9. doi: 10.1073/pnas.1415541112. Epub 2015 Apr 6.
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.
Zfp57是一个维持基因组印记的母源-合子效应基因。在此我们报告,Zfp57突变体表现出多种心脏缺陷,包括房间隔缺损(ASD)、室间隔缺损(VSD)、心肌变薄和小梁形成减少。Zfp57母源-合子突变胚胎比合子突变胚胎表现出更严重的表型且具有更高的外显率。心脏祖细胞在Zfp57突变体中表现出增殖和分化缺陷。ZFP57是基因组印记的主要调节因子,因此在没有ZFP57的胚胎心脏中DNA甲基化印记丢失。有趣的是,ZFP57的靶标印记基因DLK1的存在与心脏细胞中的NOTCH1激活相关。这些结果表明,ZFP57可能在心脏发育过程中调节NOTCH信号通路。事实上,ZFP57的缺失导致胚胎心脏中NOTCH1激活的丧失,在母源-合子突变体中观察到更严重的丧失。Zfp57的母源和合子功能似乎在NOTCH1激活和心肌细胞分化中发挥冗余作用。这是一个母源效应影响哺乳动物器官发育的例子。它还将基因组印记与NOTCH信号通路及特定的发育功能联系起来。