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本文引用的文献

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An Nkx2-5/Bmp2/Smad1 negative feedback loop controls heart progenitor specification and proliferation.一个Nkx2-5/Bmp2/Smad1负反馈回路控制心脏祖细胞的特化和增殖。
Cell. 2007 Mar 9;128(5):947-59. doi: 10.1016/j.cell.2007.01.042.
2
MEF2C transcription factor controls chondrocyte hypertrophy and bone development.MEF2C转录因子控制软骨细胞肥大和骨骼发育。
Dev Cell. 2007 Mar;12(3):377-89. doi: 10.1016/j.devcel.2007.02.004.
3
MEF2C is required for the normal allocation of cells between the ventricular and sinoatrial precursors of the primary heart field.MEF2C是原肠心脏场的心室和窦房结前体细胞正常分配所必需的。
Dev Dyn. 2006 Jul;235(7):1809-21. doi: 10.1002/dvdy.20828.
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Cardiac-specific deletion of Gata4 reveals its requirement for hypertrophy, compensation, and myocyte viability.心脏特异性缺失Gata4揭示了其对心肌肥大、代偿和心肌细胞存活的必要性。
Circ Res. 2006 Mar 31;98(6):837-45. doi: 10.1161/01.RES.0000215985.18538.c4. Epub 2006 Mar 2.
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The right ventricle, outflow tract, and ventricular septum comprise a restricted expression domain within the secondary/anterior heart field.右心室、流出道和室间隔在次级/前心脏区域内构成一个受限的表达域。
Dev Biol. 2005 Nov 1;287(1):134-45. doi: 10.1016/j.ydbio.2005.08.041. Epub 2005 Sep 26.
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Generation of conditional Mef2cloxP/loxP mice for temporal- and tissue-specific analyses.用于时间和组织特异性分析的条件性Mef2c loxP/loxP小鼠的产生。
Genesis. 2005 Sep;43(1):43-8. doi: 10.1002/gene.20152.
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Cooperative activation of atrial naturetic peptide promoter by dHAND and MEF2C.dHAND和MEF2C对心房利钠肽启动子的协同激活作用。
J Cell Biochem. 2004 Dec 15;93(6):1255-66. doi: 10.1002/jcb.20225.
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Tumor formation in p53 mutant ovaries transplanted into wild-type female hosts.将p53突变型卵巢移植到野生型雌性宿主中时的肿瘤形成。
Oncogene. 2004 Oct 7;23(46):7722-5. doi: 10.1038/sj.onc.1208037.
9
GATA-4 and MEF2C transcription factors control the tissue-specific expression of the alphaT-catenin gene CTNNA3.GATA-4和MEF2C转录因子控制αT-连环蛋白基因CTNNA3的组织特异性表达。
Nucleic Acids Res. 2004 Aug 9;32(14):4155-65. doi: 10.1093/nar/gkh727. Print 2004.
10
Isl1 identifies a cardiac progenitor population that proliferates prior to differentiation and contributes a majority of cells to the heart.Isl1可识别出一种心脏祖细胞群体，该群体在分化之前进行增殖，并为心脏贡献了大部分细胞。
Dev Cell. 2003 Dec;5(6):877-89. doi: 10.1016/s1534-5807(03)00363-0.

心脏发育过程中Nkx2.5和Mef2c转录因子的协同相互作用。

Cooperative interaction of Nkx2.5 and Mef2c transcription factors during heart development.

作者信息

Vincentz Joshua W, Barnes Ralston M, Firulli Beth A, Conway Simon J, Firulli Anthony B

机构信息

Riley Heart Research Center, Herman B Wells Center for Pediatric Research Division of Pediatrics Cardiology, Department of Anatomy, Indiana Medical School, Indianapolis, Indiana 46202-5225, USA.

出版信息

Dev Dyn. 2008 Dec;237(12):3809-19. doi: 10.1002/dvdy.21803.

DOI:10.1002/dvdy.21803
PMID:19035347
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2639719/
Abstract

The interactions of diverse transcription factors mediate the molecular programs that regulate mammalian heart development. Among these, Nkx2.5 and the Mef2c regulate common downstream targets and exhibit striking phenotypic similarities when disrupted, suggesting a potential interaction during heart development. Co-immunoprecipitation and mammalian two-hybrid experiments revealed a direct molecular interaction between Nkx2.5 and Mef2c. Assessment of mRNA expression verified spatiotemporal cardiac coexpression. Finally, genetic interaction studies employing histological and molecular analyses showed that, although Nkx2.5(-/-) and Mef2c(-/-) individual mutants both have identifiable ventricles, Nkx2.5(-/-);Mef2c(-/-) double mutants do not, and that mutant cardiomyocytes express only atrial and second heart field markers. Molecular marker and cell death and proliferation analyses provide evidence that ventricular hypoplasia is the result of defective ventricular cell differentiation. Collectively, these data support a hypothesis where physical, functional, and genetic interactions between Nkx2.5 and Mef2c are necessary for ventricle formation.

摘要

多种转录因子的相互作用介导了调控哺乳动物心脏发育的分子程序。其中，Nkx2.5和Mef2c调控共同的下游靶点，并且在功能缺失时表现出惊人的表型相似性，这表明它们在心脏发育过程中可能存在相互作用。免疫共沉淀和哺乳动物双杂交实验揭示了Nkx2.5和Mef2c之间存在直接的分子相互作用。对mRNA表达的评估证实了两者在心脏中的时空共表达。最后，采用组织学和分子分析的遗传相互作用研究表明，尽管Nkx2.5(-/-)和Mef2c(-/-)单个突变体都有可识别的心室，但Nkx2.5(-/-);Mef2c(-/-)双突变体却没有，并且突变的心肌细胞仅表达心房和第二心脏场标志物。分子标志物以及细胞死亡和增殖分析提供了证据，表明心室发育不全是心室细胞分化缺陷的结果。总的来说，这些数据支持了一个假说，即Nkx2.5和Mef2c之间的物理、功能和遗传相互作用是心室形成所必需的。