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. 2014 Nov 26;1(1):e970883. doi: 10.4161/23262125.2014.970883

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© 2014 The Author(s). Published with license by Taylor & Francis Group, LLC

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 7. — Blocking histone deacetylation rescues the ability of neural precursors to form clones. (A) Representative micrographs of coronal telencephalic sections obtained from control E13.5 embryos showing the effect of TSA on the levels and distribution of acetylated histone 3 (AcH3), acetylated histone 4 (AcH4) and histone 3 (H3) immunoreactivity in the GE and in the cortex. Pregnant females were injected with TSA at 11 d.p.c. and every 12h for 48h before analysis. V = Ventricle. Scale bar is 30 mM. (B) Quantitative analyses of the number of primary clones obtained from EGFR^high and EGFR^low cells isolated at DIV 1 cultures established from E13.5 embryos with the indicated genotypes after TSA treatment.