CDK7 and miR-210 Co-regulate Cell-Cycle Progression of Neural Progenitors in the Developing Neocortex Academic Article uri icon


MeSH Major

  • Brain Neoplasms
  • DNA-Binding Proteins
  • Glioma
  • Polymorphism, Single Nucleotide


  • The molecular mechanisms regulating neural progenitor (NP) proliferation are fundamental in establishing the cytoarchitecture of the mammalian neocortex. The rate of cell-cycle progression and a fine-tuned balance between cell-cycle re-entry and exit determine the numbers of both NPs and neurons as well as postmitotic neuronal laminar distribution in the cortical wall. Here, we demonstrate that the microRNA (miRNA) miR-210 is required for normal mouse NP cell-cycle progression. Overexpression of miR-210 promotes premature cell-cycle exit and terminal differentiation in NPs, resulting in an increase in early-born postmitotic neurons. Conversely, miR-210 knockdown promotes an increase in the radial glial cell population and delayed differentiation, resulting in an increase in late-born postmitotic neurons. Moreover, the cyclin-dependent kinase CDK7 is regulated by miR-210 and is necessary for normal NP cell-cycle progression. Our findings demonstrate that miRNAs are essential for normal NP proliferation and cell-cycle progress during neocortical development.

publication date

  • July 12, 2016



  • Academic Article



  • eng

PubMed Central ID

  • PMC4944761

Digital Object Identifier (DOI)

  • 10.1016/j.stemcr.2016.06.005

PubMed ID

  • 27411104

Additional Document Info

start page

  • 69

end page

  • 79


  • 7


  • 1