Journal
CELL REPORTS
Volume 12, Issue 5, Pages 760-773Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2015.06.074
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Funding
- NIH [T32 HD007263, F32 HD070572, R01 GM101180, U54 HD055764, R01 NS34661, R01 DE016402]
- California Institute of Regenerative Medicine [RN2-00906-1]
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The evolutionarily conserved miR-302 family of microRNAs is expressed during early mammalian embryonic development. Here, we report that deletion of miR-302a-d in mice results in a fully penetrant late embryonic lethal phenotype. Knockout embryos have an anterior neural tube closure defect associated with a thickened neuroepithelium. The neuroepithelium shows increased progenitor proliferation, decreased cell death, and precocious neuronal differentiation. mRNA profiling at multiple time points during neurulation uncovers a complex pattern of changing targets over time. Overexpression of one of these targets, Fgf15, in the neuroepithelium of the chick embryo induces precocious neuronal differentiation. Compound mutants between mir302 and the related mir-290 locus have a synthetic lethal phenotype prior to neurulation. Our results show that mir-302 helps regulate neurulation by suppressing neural progenitor expansion and precocious differentiation. Furthermore, these results uncover redundant roles for mir-290 and mir-302 early in development.
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