MTGR1 对 NEUROG2 活性的反馈调节是神经发生进展所必需的。
Feedback regulation of NEUROG2 activity by MTGR1 is required for progression of neurogenesis.
机构信息
Department of Neuroscience and Stem Cell Institute, University of Minnesota, 6-145 Jackson Hall, 321 Church St. SE, Minneapolis, MN 55455, USA.
出版信息
Mol Cell Neurosci. 2009 Dec;42(4):267-77. doi: 10.1016/j.mcn.2009.07.011. Epub 2009 Jul 28.
The sequential steps of neurogenesis are characterized by highly choreographed changes in transcription factor activity. In contrast to the well-studied mechanisms of transcription factor activation during neurogenesis, much less is understood regarding how such activity is terminated. We previously showed that MTGR1, a member of the MTG family of transcriptional repressors, is strongly induced by a proneural basic helix-loop-helix transcription factor, NEUROG2 in developing nervous system. In this study, we describe a novel feedback regulation of NEUROG2 activity by MTGR1. We show that MTGR1 physically interacts with NEUROG2 and represses transcriptional activity of NEUROG2. MTGR1 also prevents DNA binding of the NEUROG2/E47 complex. In addition, we provide evidence that proper termination of NEUROG2 activity by MTGR1 is necessary for normal progression of neurogenesis in the developing spinal cord. These results highlight the importance of feedback regulation of proneural gene activity in neurodevelopment.
神经发生的顺序步骤的特点是转录因子活性的高度协调变化。与神经发生过程中转录因子激活的研究良好的机制相比，人们对这种活性如何终止知之甚少。我们之前表明，MTG 家族转录抑制剂 MTGR1 在内源性神经发生过程中受到神经前体细胞碱性螺旋-环-螺旋转录因子 NEUROG2 的强烈诱导。在这项研究中，我们描述了 MTGR1 对 NEUROG2 活性的一种新的反馈调节。我们表明 MTGR1 与 NEUROG2 相互作用，并抑制 NEUROG2 的转录活性。MTGR1 还阻止了 NEUROG2/E47 复合物的 DNA 结合。此外，我们提供的证据表明，MTGR1 通过适当终止 NEUROG2 活性对于发育中脊髓中的神经发生的正常进展是必要的。这些结果强调了神经发育中神经前体细胞基因活性的反馈调节的重要性。
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