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. 2016 Apr 20;7:11349. doi: 10.1038/ncomms11349

Figure 5. Co-electroporation of Cdk inhibitor p18 and NICD inhibit cell-cycle progression of progenitors while maintaining them in an undifferentiated state.

Figure 5

(a) Experimental design. pCAG::EGFP-3NLS alone (control), or with pCAG::NICD, or with both pCAG::NICD and pEF::p18 was electroporated into E11 cerebral wall in vivo. At E14, BrdU was administered for 30 min, and brains were fixed and stained with antibodies to EGFP, BrdU (b,c), PH3 (d), BLBP (f), Nestin (g), Ki67 (h), Pax6 (i), Sox2 (j) or Tbr2 (k). (c,d) Frequency of BrdU+ cells (c) or PH3+ cells (d) in the EGFP+VZ cells was significantly reduced relative to the control by NICD/p18 co-overexpression (c, N=4 for each case; d, N=5 for each case; Mann–Whitney U test, means±s.d.). The characterization of the EGFP+ cells in the IZ/SVZ and CP is presented in Supplementary Fig. 11. (e–g) NICD/p18 co-expressing cells have radially elongated fibres that are positive for BLBP and Nestin. pCAG::EGFP, pCAG::NICD and pEF::p18 were co-electroporated on E11, and the brains were examined at E14. (h–l) Most of the NICD/p18 co-expressing cells in the VZ are negative for Ki67 and Tbr2 and positive for Pax6 and Sox2. Bars, 20 μm in (b), 60 μm in (e), 30 μm in (f,g), 40 μm in (h–k).