Suppr超能文献

母体和合子的Zfp57在心脏发育中调节NOTCH信号通路。

Maternal and zygotic Zfp57 modulate NOTCH signaling in cardiac development.

作者信息

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

机构信息

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.

出版信息

Proc Natl Acad Sci U S A. 2015 Apr 21;112(16):E2020-9. doi: 10.1073/pnas.1415541112. Epub 2015 Apr 6.

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.

摘要

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。

相似文献

1
Maternal and zygotic Zfp57 modulate NOTCH signaling in cardiac development.
Proc Natl Acad Sci U S A. 2015 Apr 21;112(16):E2020-9. doi: 10.1073/pnas.1415541112. Epub 2015 Apr 6.
2
Extending the maternal-zygotic effect with genomic imprinting.
Mol Hum Reprod. 2010 Sep;16(9):695-703. doi: 10.1093/molehr/gaq028. Epub 2010 Apr 9.
3
ZFP57 dictates allelic expression switch of target imprinted genes.
Proc Natl Acad Sci U S A. 2021 Feb 2;118(5). doi: 10.1073/pnas.2005377118.
4
Maternal and zygotic ZFP57 regulate coronary vascular formation and myocardium maturation in mouse embryo.
Dev Dyn. 2024 Jan;253(1):144-156. doi: 10.1002/dvdy.530. Epub 2022 Sep 10.
5
A maternal-zygotic effect gene, Zfp57, maintains both maternal and paternal imprints.
Dev Cell. 2008 Oct;15(4):547-57. doi: 10.1016/j.devcel.2008.08.014.
7
Exerts Maternal and Sexually Dimorphic Effects on Genomic Imprinting.
Front Cell Dev Biol. 2022 Feb 2;10:784128. doi: 10.3389/fcell.2022.784128. eCollection 2022.
9
WD40 repeat and FYVE domain containing 3 is essential for cardiac development.
Cardiovasc Res. 2019 Jul 1;115(8):1320-1331. doi: 10.1093/cvr/cvy285.

引用本文的文献

1
LncRNAs in the Domain Are Essential for Mid-Embryonic Heart Development.
Int J Mol Sci. 2024 Jul 26;25(15):8184. doi: 10.3390/ijms25158184.
4
Developmental toxicant exposures and sex-specific effects on epigenetic programming and cardiovascular health across generations.
Environ Epigenet. 2022 Oct 3;8(1):dvac017. doi: 10.1093/eep/dvac017. eCollection 2022.
5
Exerts Maternal and Sexually Dimorphic Effects on Genomic Imprinting.
Front Cell Dev Biol. 2022 Feb 2;10:784128. doi: 10.3389/fcell.2022.784128. eCollection 2022.
7
Maternal effect genes: Update and review of evidence for a link with birth defects.
HGG Adv. 2021 Oct 16;3(1):100067. doi: 10.1016/j.xhgg.2021.100067. eCollection 2022 Jan 13.
8
ZFP57 dictates allelic expression switch of target imprinted genes.
Proc Natl Acad Sci U S A. 2021 Feb 2;118(5). doi: 10.1073/pnas.2005377118.
10
DNA Methylation Readers and Cancer: Mechanistic and Therapeutic Applications.
Front Oncol. 2019 Jun 11;9:489. doi: 10.3389/fonc.2019.00489. eCollection 2019.

本文引用的文献

1
Multiple Dlk1 splice variants are expressed during early mouse embryogenesis.
Int J Dev Biol. 2014;58(1):65-70. doi: 10.1387/ijdb.130316sc.
2
Dlk1 promotes a fast motor neuron biophysical signature required for peak force execution.
Science. 2014 Mar 14;343(6176):1264-6. doi: 10.1126/science.1246448.
3
DLK1 promotes lung cancer cell invasion through upregulation of MMP9 expression depending on Notch signaling.
PLoS One. 2014 Mar 12;9(3):e91509. doi: 10.1371/journal.pone.0091509. eCollection 2014.
4
MicroRNA-126-5p promotes endothelial proliferation and limits atherosclerosis by suppressing Dlk1.
Nat Med. 2014 Apr;20(4):368-76. doi: 10.1038/nm.3487. Epub 2014 Mar 2.
5
Membrane-bound delta-like 1 homolog (Dlk1) promotes while soluble Dlk1 inhibits myogenesis in C2C12 cells.
FEBS Lett. 2014 Apr 2;588(7):1100-8. doi: 10.1016/j.febslet.2014.02.027. Epub 2014 Feb 26.
6
Preadipocytes proliferate and differentiate under the guidance of Delta-like 1 homolog (DLK1).
Adipocyte. 2013 Oct 1;2(4):272-5. doi: 10.4161/adip.24994. Epub 2013 May 13.
7
Dual role of delta-like 1 homolog (DLK1) in skeletal muscle development and adult muscle regeneration.
Development. 2013 Sep;140(18):3743-53. doi: 10.1242/dev.095810. Epub 2013 Aug 14.
8
De novo mutations in histone-modifying genes in congenital heart disease.
Nature. 2013 Jun 13;498(7453):220-3. doi: 10.1038/nature12141. Epub 2013 May 12.
9
Genetics of congenital heart disease: the glass half empty.
Circ Res. 2013 Feb 15;112(4):707-20. doi: 10.1161/CIRCRESAHA.112.300853.
10
Notch signaling: genetics and structure.
WormBook. 2013 Jan 17:1-28. doi: 10.1895/wormbook.1.10.2.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验