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活动诱导的DNA断裂控制神经元早期反应基因的表达

Ram Madabhushi¹, Fan Gao¹, Andreas R Pfenning²

¹Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

|June 9, 2015

概括

神经元活动触发了基因促进器中的DNA双链断裂 (DSB),这对学习和记忆至关重要. 这种DNA损伤反应由托波异粒酶IIβ介导,促进基因表达.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

神经元活动迅速诱导即时早期的基因,对突触可塑性,学习和记忆至关重要.
了解神经元刺激的基因调节背后的分子机制至关重要.

研究的目的:

研究DNA双链断裂 (DSB) 在神经元活动后的早期基因表达的调节中的作用.
确定参与活动依赖的DSB形成的分子参与者及其功能后果.

主要方法:

分子生物学技术分子生物学技术.
全基因组的下一代测序.
使用拓二酶IIβ (Topo IIβ) 的基因淘汰研究.

主要成果:

神经元活动刺激会诱导Fos,Npas4和Egr1.1等关键早期反应基因的促进子区域的DNA双链断裂 (DSB).
针对Fos和Npas4促进体中DSBs的向诱导可以独立于外部刺激来驱动基因表达.
拓糖酶IIβ (Topo IIβ) 调解了活动依赖的DSB形成,因为它的敲除在刺激时减少了DSB和基因表达.

结论:

DNA双链断裂 (DSBs) 是神经元中的一种生理机制,可以迅速克服基因表达的拓障碍.
托波IIβ在通过活动诱导的DSB形成促进早期反应基因表达方面发挥着关键作用.
这些发现揭示了一种新的调节途径,将神经元活动,DNA损伤和基因表达联系起来,这对于认知功能至关重要.

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