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首页> 外文期刊>Developmental cell >A Self-Organizing miR-132/Ctbp2 Circuit Regulates Bimodal Notch Signals and Glial Progenitor Fate Choice during Spinal Cord Maturation
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A Self-Organizing miR-132/Ctbp2 Circuit Regulates Bimodal Notch Signals and Glial Progenitor Fate Choice during Spinal Cord Maturation

机译：自组织的miR-132 / Ctbp2电路可调节脊髓成熟过程中的双峰Notch信号和神经胶质祖细胞的命运选择。

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摘要

Radial glial progenitors play pivotal roles in the development and patterning of the spinal cord, and their fate is controlled by Notch signaling. How Notch is shaped to regulate their crucial transition from expansion toward differentiation remains, however, unknown. miR-132 in the developing zebrafish dampens Notch signaling via a cascade involving the transcriptional corepressor Ctbp2 and the Notch suppressor Sirt1. At early embryonic stages, high Ctbp2 levels sustain Notch signaling and radial glial expansion and concomitantly induce miR-132 expression via a double-negative feedback loop involving Rest inhibition. The changing balance in miR-132 and Ctbp2 interaction gradually drives the switch in Notch output and radial glial progenitor fate as part of the larger developmental program involved in the transition from embryonic to larval spinal cord.
机译：ial神经胶质祖细胞在脊髓的发育和模式中起关键作用，其命运受Notch信号的控制。 Notch的形状如何调节其从扩张到分化的关键过渡，但是仍然未知。发育中的斑马鱼中的miR-132通过涉及转录共抑制物Ctbp2和Notch抑制子Sirt1的级联抑制Notch信号传导。在早期胚胎阶段，高Ctbp2水平维持Notch信号传导和放射状神经胶质细胞扩张，并通过涉及Rest抑制的双负反馈回路同时诱导miR-132表达。 miR-132和Ctbp2相互作用中不断变化的平衡逐渐推动了Notch输出和radial神经胶质祖细胞命运的转变，这是涉及从胚胎到幼虫脊髓转变的较大发育计划的一部分。

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