The microRNA miR-124 antagonizes the anti-neural REST/SCP1 pathway during embryonic CNS development.
By J. Visvanathan, Seunghee Lee, Bora Lee, Jae W. Lee, Soo-Kyung Lee. Genes & Development, 2007
694 citations recorded by the source corpus.
Neuronal gene expression is tightly regulated in developing CNS. Here, we demonstrate the anti-neural function of phosphatase SCP1 (small C-terminal domain phosphatase 1) during development. We further show that the neuron-enriched microRNA miR-124 directly targets SCP1-3' untranslated region (UTR) to suppress SCP1 expression. In developing spinal cord, expression of miR-124 and SCP1 is complementary, and miR-124 antagonism phenocopies SCP1 overexpression and vice versa. In P19 cells, miR-124 suppresses SCP1 expression and induces neurogenesis, and SCP1 counteracts this proneural activity of miR-124. Our results suggest that, during CNS development, timely down-regulation of SCP1 is critical for inducing neurogenesis, and miR-124 contributes to this process at least in part by down-regulating SCP1 expression.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/f3220aa8454c85c81b1ed52703044febe4ab7708
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Citations in the corpus
- The MicroRNA miR-124 promotes neuronal differentiation by triggering brain-specific alternative pre-mRNA splicing. (2007, background): “As previously mentioned, miR124 was recently shown to target SCP1 mRNA during neuronal differentiation (Visvanathan et al., 2007).”
- miRecords: an integrated resource for microRNA–target interactions (2008, background): “The authors fused the cog-1 30UTR to a green fluorescent protein (GFP) sensor construct, and found that this fusion was effectively downregulated in ASEL but not in ASER.”
- MicroRNAs in development and disease. (2011, background): “Controversially, another study showed that overexpression of miR-124 enhanced neurogenesis in the same model via suppression of synaptonemal complex protein 1 (SCP1), an anti-neural factor that is recruited by REST (637).”