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. 2020 Aug 31;10:14331. doi: 10.1038/s41598-020-71229-x

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Validation of inducible conditional H2A.Z knockout. (a) Design used to induce H2A.Z deletion in CamKIIα-positive neurons in adult mice. All mice were floxed for H2afz and H2afv. Conditional knockout was induced by crossing floxed mice with CamKIIα-CreER mice, such that Cre positive (Cre⁺) mice exhibited H2A.Z deletion upon treatment with tamoxifen, whereas Cre negative (Cre^-) mice treated with tamoxifen served as controls. (b) The deletion of each H2A.Z-encoding gene was validated by qPCR at the mRNA level. N = 10–12/group; (c) reduced protein was validated using immunoblotting for total H2A.Z in the hippocampus. N = 6/group; (d) reduced H2A.Z binding was validated using H2A.Z ChIP; (e) Preservation of nucleosomes was validated using histone H3 ChIP N = 6/group. Data are shown as Mean ± SEM, *p ≤ 0.05.