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Figure 3 | Neural Development

Figure 3

From: Multiple non-cell-autonomous defects underlie neocortical callosal dysgenesis in Nfib-deficient mice

Figure 3

Normal proliferation and cell death at the cortical midline of mice lacking Nfib. (A, B) Proliferation at the cortical midline in wildtype (A) and Nfib-deficient (B) mice was assessed with immunohistochemistry against the mitotic marker phosphohistone H3. (C) Counts of phosphohistone H3-positive cells at the cortical midline demonstrated that there was no significant difference in proliferation between Nfib null mutants and controls at E13, E14 or E15. (D, E) Apoptosis at the midline in wildtype (D) and Nfib-deficient (E) brains was assessed via expression of the marker for cell death, cleaved caspase 3. There were few apoptotic cells observed in either wildtype or knockout samples (arrows in (D, E)), and these were predominantly observed around the area where fusion between the cerebral hemispheres occurs. (F) We did not observe any significant differences in the numbers of apoptotic cells in mice lacking Nfib compared to wildtype controls at E14, E15 or E18. n = 3 independent replicates for both wildtype and Nfib mutants. Error bars indicate standard error of the mean. Scale bar: 300 μm.

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