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. 2019 Oct 5;47(20):10612–10627. doi: 10.1093/nar/gkz816

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© The Author(s) 2019. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 1. — B cell development is unaffected by CD19-cre driven deletion of Hdac3. (A) Loss of Hdac3 protein was determined by western blot analyses of proteins isolated from B220⁺ splenocytes of Hdac3^+/+CD19cre^+/−(WT) controls or Hdac3^F/−CD19cre^+/−(Hdac3^−/−) animals. (B) Flow cytometric analysis utilizing IgM and B220 antibodies characterizes B cell development within the bone marrow of control and Hdac3-deleted mice. Graphical representation of B cell populations as a percentage of the total bone marrow from at least 6 mice per group is presented at the right. (C) Flow cytometry was used to determine the number of B220⁺ cells per spleen from multiple mice. (D) In order to characterize the structure of splenic follicles, formalin-fixed spleens were subject to H&E staining and immunohistochemistry with α-B220. (E) Flow cytometric characterization of splenic B cell populations was carried out. B220⁺ splenocytes were further analyzed based on surface CD23 and CD21 expression. Graph on right depicts five WT mice and four Hdac3^−/− mice.