...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neuron >Control of cognition and adaptive behavior by the GLP/G9a epigenetic suppressor complex.
【24h】

Control of cognition and adaptive behavior by the GLP/G9a epigenetic suppressor complex.

机译：通过GLP / G9a表观遗传抑制复合物控制认知和适应行为。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The genetic basis of cognition and behavioral adaptation to the environment remains poorly understood. Here we demonstrate that the histone methyltransferase complex GLP/G9a controls cognition and adaptive responses in a region-specific fashion in the adult brain. Using conditional mutagenesis in mice, we show that postnatal, neuron-specific deficiency of GLP/G9a leads to derepression of numerous nonneuronal and neuron progenitor genes in adult neurons. This transcriptional alteration is associated with complex behavioral abnormalities, including defects in learning, motivation, and environmental adaptation. The behavioral changes triggered by GLP/G9a deficiency are similar to key symptoms of the human 9q34 mental retardation syndrome that is associated with structural alterations of the GLP/EHMT1 gene. The likely causal role of GLP/G9a in mental retardation in mice and humans suggests a key role for the GLP/G9a-controlled histone H3K9 dimethylation in regulation of brain function through maintenance of the transcriptional homeostasis in adult neurons.
机译：认知和行为适应环境的遗传基础仍然知之甚少。在这里，我们证明了组蛋白甲基转移酶复合物GLP / G9a在成人大脑中以区域特定的方式控制认知和适应性反应。使用小鼠中的条件诱变，我们显示GLP / G9a的出生后，神经元特异性缺陷导致成年神经元中许多非神经元和神经元祖基因的抑制。这种转录改变与复杂的行为异常有关，包括学习，动机和环境适应方面的缺陷。 GLP / G9a缺乏症引发的行为变化与人类9q34智力低下综合征的关键症状相似，后者与GLP / EHMT1基因的结构改变有关。 GLP / G9a可能在小鼠和人类的智力发育迟缓中起因作用，这表明GLP / G9a控制的组蛋白H3K9二甲基化通过维持成年神经元的转录稳态而在调节脑功能中起着关键作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号