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miR-302 Is Required for Timing of Neural Differentiation, Neural Tube Closure, and Embryonic Viability

  • Author(s): Parchem, RJ
  • Moore, N
  • Fish, JL
  • Parchem, JG
  • Braga, TT
  • Shenoy, A
  • Oldham, MC
  • Rubenstein, JLR
  • Schneider, RA
  • Blelloch, R
  • et al.

Published Web Location

http://dx.doi.org/10.1016/j.celrep.2015.06.074
No data is associated with this publication.
Abstract

© 2015 The Authors. 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.

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