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Fig. 3 | Molecular Brain

Fig. 3

From: Fstl1 is involved in the regulation of radial glial scaffold development

Fig. 3

Loss of Fstl1 results in aberrant positioning of upper-layer cortical neurons. a to b’ Although similar distributions of E12.5-born cells are observed in the WT (a) and Fstl1 −/− (a’) cortices, a greater fraction of cell born at E14.5 (b’) are found in deeper cortical layers in the Fstl1 −/− cortices compared to the WT cortices (b). The percentages of cells in the upper layers (bins 8–10) and IZ (bins 2–4) are indicated in the histograms. n = 3 per genotype per experimental condition. *p < 0.05, ** p < 0.01. The error bars represent the s.e.m. c and c’ The migration of early-born deeper-layer neurons is unchanged in the Fstl1 −/− cortex (c) compared to that in the WT cortex (d). BrdU was injected at E12.5, and the brains were then harvested at E14.5. d to e’ The number of BrdU+ cells was similar in the WT (d and e) and Fstl1 −/− cortices (d’ and e’) at E14.5 (d and d’) and E16.5 (e and e’). f and g The number of BrdU+ progenitor cells per entire cortical section at E14.5 (f) and E16.5 (g). The data are the mean ± s.e.m. At E14.5, 172.4 ± 5.1 for WT, n = 5; and 173.5 ± 7.2 for Fstl1 −/−, n = 5, p = 0.91. At E16.5, 69.5 ± 2.4 for WT, n = 3; and 73.5 ± 2.1 for Fstl1 −/−, n = 3, p = 0.28. h to i’ Immunolabelling with anti-Ki67 (h and h’) and anti-pHH3 (i and i’) antibodies confirmed that the proliferation of progenitor cells was not obviously changed at E16.5. Scale bars: 100 μm

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