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. 2013 Sep 1;27(17):1903–1916. doi: 10.1101/gad.219899.113

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© 2013, Published by Cold Spring Harbor Laboratory Press

This article, published in Genes & Development, is available under a Creative Commons License (Attribution-NonCommercial 3.0 Unported), as described at http://creativecommons.org/licenses/by-nc/3.0/.

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Figure 1. — PRMT5 deficiency in the CNS results in early postnatal lethality. Nestin-Cre-induced deletion of the PRMT5 gene in the CNS. (A) Weight in milligrams of wild-type (Prmt5^F/F) and Prmt5-deleted (Prmt5^F/FNes) brains at three different time points (E17.5, P0, and P10). Brain sizes of P10 Prmt5^F/F and Prmt5^F/FNes mice are shown as an example in the right panel. (B) Hematoxylin and eosin (H&E)-stained sagittal and coronal sections of P10 cerebrum (Cr) and the cerebellum (Cb) from Prmt5^F/F (right) and Prmt5^F/FNes (left). (C) Coronal sections of P0 brains. Cellularity of the cortical plate (CP) and VZ/SVZ are indicated in wild-type (wt; black) and mutant (red) brains. (MZ) Marginal zone; (SP) subplate; (IZ) intermediate zone. (D) SOX2 and Ki67 immunohistochemistry (IHC) staining in P0 brains. (E) Cleaved Caspase 3 (CC3) staining is shown in both the cortex and the gangliomic eminence.