Control of mouse cardiac morphogenesis and myogenesis by transcription factor MEF2C
Control of mouse cardiac morphogenesis and myogenesis by transcription factor MEF2C
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DOI：
10.1126/science.276.5317.1404
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发表时间：
1997-05-30
期刊：
影响因子：
56.9
通讯作者：
Olson, EN
中科院分区：
文献类型：
--
作者：
Lin, Q;Schwarz, J;Olson, EN
MADS（MCM 1，无配偶，缺乏，血清反应因子）盒转录因子的肌细胞增强因子-2（MEF 2）家族成员结合与肌肉特异性基因相关的富含A-T的DNA序列。小鼠MEF 2C基因在线性心管形成之前在心脏前体细胞中表达。在MEF 2C无效突变的纯合子小鼠中，心管没有经历成环形态发生，未来的右心室没有形成，并且心肌基因的子集没有表达。突变心脏右心室区域的缺失与dHAND基因的下调相关，dHAND基因编码心脏形态发生所需的基本螺旋-环-螺旋转录因子。因此，MEF 2C是心肌发生和右心室发育的重要调节因子。
Members of the myocyte enhancer factor-2 (MEF2) family of MADS (MCM1, agamous, deficiens, serum response factor)-box transcription factors bind an A-T-rich DNA sequence associated with muscle-specific genes. The murine MEF2C gene is expressed in heart precursor cells before formation of the linear heart tube, In mice homozygous for a null mutation of MEF2C, the heart tube did not undergo looping morphogenesis, the future right ventricle did not form, and a subset of cardiac muscle genes was not expressed. The absence of the right ventricular region of the mutant heart correlated with down-regulation of the dHAND gene, which encodes a basic helix-loop-helix transcription factor required for cardiac morphogenesis. Thus, MEF2C is an essential regulator of cardiac myogenesis and right ventricular development.