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. 2011 Dec 22;5(3):351–365. doi: 10.1242/dmm.002873

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© 2012. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms

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Fig. 6. — Sall1 regulates cell cycle exit. Quantification of VZ and SVZ cell number at E11.5, E12.5, E14.5, E17.5 and E18.5 in control and Sall1^−/− mice (A). The labeling index was not altered in Sall1-deficient animals at E11.5, E14.5 or E17.5 compared with controls (B). The rate of neuronal differentiation (Q fraction) was increased at E11.5 (E12.5: BrdU injected at E11.5), but decreased at E14.5 (E15.5: BrdU injected at E14.5) and E17.5 (E18.5: BrdU injected at E17.5) in Sall1^−/− animals compared with controls (C). Quantification of Tbr2 cell number at E14.5, E17.5 and E18.5 (D). Alterations in the rate of VZ (Pax6+) and SVZ (Tbr2+) cell cycle re-entry in Sall1^−/−animals compared with controls at E14.5 and E17.5 (E). *, P<0.05; **, P<0.01; ***, P<0.001.