Regulation of Olig2 in Motor Neuron Development

Olig2 在运动神经元发育中的调节

• 批准号: 7468016
• 负责人: Brian P Hafler
• 金额: $ 2万
• 依托单位: HARVARD MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-07-01 至 2009-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7468016
• 关键词: Address; Binding; Development; Disease; Elements; Embryo; Enhancers; Fellowship; Genes; Human; Mammals; Motor Neurons; Mus; National Research Service Awards; Neuraxis; Neuroglia; Neurologic; Neurons; Oligodendroglia; Pattern Formation; Regulation; Regulatory Element; Reporter; Research; Role; Sequence Deletion; Spinal Cord; Staging; Testing; Transgenic Mice; deletion analysis; nervous system development; neurodevelopment; progenitor; relating to nervous system; repaired; research study; transcription factor

DESCRIPTION (provided by applicant): The bHLH transcription factor-encoding genes, Olig1 and Olig2, have essential roles during central nervous system (CNS) development. In the spinal cord, Olig2 is required for pattern formation specification of motor neurons and oligodendrocytes. In this Kirschstein National Research Service Award Fellowship Application, I propose studies intended to yield a detailed understanding of Olig2 regulation during early stages of neural development. Recently, we have identified a 3.6 kb regulatory element that governs Olig2 expression specifically in motor neuron progenitors. The mechanism by which this enhancer regulates expression of Olig2 is unknown. My objective is to identify trans-acting transcription factors that interact with the enhancer. This research will address fundamental issues of neural pattern formation and neuronal versus glial cell fate specification. These experiments directly address issues in mammals related to regrowth and eventually the repair of neural elements destroyed in neurologic diseases.

描述（由申请人提供）： bHLH 转录因子编码基因 Olig1 和 Olig2 在中枢神经系统 (CNS) 发育过程中发挥重要作用。在脊髓中，运动神经元和少突胶质细胞的模式形成规范需要 Olig2。在这份 Kirschstein 国家研究服务奖奖学金申请中，我提出了旨在详细了解神经发育早期阶段 Olig2 调节的研究。最近，我们发现了一个 3.6 kb 的调控元件，它专门控制运动神经元祖细胞中的 Olig2 表达。该增强子调节 Olig2 表达的机制尚不清楚。我的目标是识别与增强子相互作用的反式作用转录因子。这项研究将解决神经模式形成和神经元与神经胶质细胞命运规范的基本问题。这些实验直接解决了哺乳动物中与神经系统疾病中受损的神经元件的再生和最终修复相关的问题。