| First Author | Parchem RJ | Year | 2015 |
| Journal | Cell Rep | Volume | 12 |
| Issue | 5 | Pages | 760-73 |
| PubMed ID | 26212322 | Mgi Jnum | J:232516 |
| Mgi Id | MGI:5779471 | Doi | 10.1016/j.celrep.2015.06.074 |
| Citation | Parchem RJ, et al. (2015) miR-302 Is Required for Timing of Neural Differentiation, Neural Tube Closure, and Embryonic Viability. Cell Rep 12(5):760-73 |
| abstractText | 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 mir-302 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. |
