Figure 3. Imp1 deficiency leads to precocious maturation of Pax6+ stem cells into Tbr2+ intermediate neuronal progenitors in the dorsal telencephalon.

(A–C) Imp1 deficiency significantly reduced the number of Pax6+ neural stem cells in the dorsomedial telencephalon (DMT) at E14.5 and E18.5, and in the dorsolateral telencephalon (DLT) at E18.5 (**p<0.05; mean ± SD for 3–4 mice/genotype at each stage with 6–8 sections/brain). Imp1 deficiency significantly reduced the percentage of Pax6+ neural stem cells that were BrdU+ in E18.5 DMT (**p<0.05; mean ± SD for 3–4 mice/genotype at each stage with 6–7 sections/brain). (D–F) Imp1 deficiency transiently increased the number of Tbr2+ intermediate progenitors in the DMT at E12.5 and E14.5, and in the DLT at E12.5 (*p<0.01; mean ± SD for 3–5 brains/genotype at each stage with 6–8 sections/brain). Imp1 deficiency did not significantly affect the percentage of Tbr2+ cells that were also BrdU+ (mean ± SD for 3–4 mice/genotype with six sections/brain).

DOI: http://dx.doi.org/10.7554/eLife.00924.009

Figure 3—figure supplement 1. Imp1 deficiency significantly reduced the percentage of proliferating Pax6+ neural stem cells in E18.5 dorsomedial telencephalon (DMT).

(A–B) DMT sections stained with antibodies against Pax6 and phospho-Histone H3 (pH3), a marker of mitotic cells. (B) Imp1 deficiency significantly reduced the percentage of Pax6+ neural stem cells that were pH3+ in E18.5 DMT but not at E12.5 or E14.5, or in DLT (**p<0.05; mean ± SD for 3–4 brains/genotype at each stage with 4–7 sections/brain). (C–D) DMT sections stained with antibodies against Tbr2 and phospho-Histone H3. (D) Imp1 deficiency did not significantly affect the percentage of Tbr2+ cells that were also pH3+ (mean ± SD for 3–4 brains/genotype with six sections/brain).

DOI: http://dx.doi.org/10.7554/eLife.00924.010