Journal
NATURE COMMUNICATIONS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms8718
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Funding
- NIH/NINDS [R01 NS054941]
- March of Dimes Foundation
- Christopher and Dana Reeve Foundation
- NIH/NIDDK [R01 DK064678, R01 DK103661]
- NIH/NIMH [R01 MH094416]
- National Research Foundation of Korea (NRF) - Korean government (MEST) [2012M3A9C6050508]
- National Research Foundation of Korea (NRF) - Korean government (MSIP) [2011-0030001]
- Aspiring Researcher Program of Seoul National University
- National Research Foundation of Korea [2012M3A9C6050508] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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While microRNAs have emerged as an important component of gene regulatory networks, it remains unclear how microRNAs collaborate with transcription factors in the gene networks that determines neuronal cell fate. Here we show that in the developing spinal cord, the expression of miR-218 is directly upregulated by the Isl1-Lhx3 complex, which drives motor neuron fate. Inhibition of miR-218 suppresses the generation of motor neurons in both chick neural tube and mouse embryonic stem cells, suggesting that miR-218 plays a crucial role in motor neuron differentiation. Results from unbiased RISC-trap screens, in vivo reporter assays and overexpression studies indicated that miR-218 directly represses transcripts that promote developmental programs for interneurons. In addition, we found that miR-218 activity is required for Isl1-Lhx3 to effectively induce motor neurons and suppress interneuron fates. Together our results reveal an essential role of miR-218 as a downstream effector of the Isl1-Lhx3 complex in establishing motor neuron identity.
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