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. 2017 Oct 11;27(2):211–223. doi: 10.1093/hmg/ddx366

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© The Author(s) 2017. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 7. — Removal of the neomycin cassette from the Velocigene Trem2 knockout mice ameliorates aberrant Treml1 expression. (A) Schematic of Trem2^−/− (Velocigene) male mice crossed with EIIA-Cre mice to remove the floxed neomycin cassette driven by the human Ubiquitin C promoter. The first cross of EIIA-Cre to Trem2^−/− (Velocigene) mice creates a mosaic of neomycin deletion due to some inefficiencies in Cre activity at early embryonic stages. (B) RT-qPCR for Treml1 levels in hippocampal tissue from EIIA-Cre^+/− Trem2^+/− mice that were negative for neomycin, were compared with WT, Trem2^+/−, and Trem2^−/− Velocigene controls. EIIA-Cre^+/− Trem2^+/− mice that were negative for neomycin had significantly decreased levels of Treml1 relative to both Trem2^+/−, and Trem2^−/− Velocigene controls and were similar to WT. Shown are the averages ± S.E.M from N = 3–5 animals per group (One-way ANOVA, Tukey posthoc, *P <0.05, ****P≤ 0.0001). (C) RT-qPCR for Treml1 and neomycin levels in hippocampal tissue from EIIA Cre^+/− Trem2^+/− mice over a range of mosaicism was conducted. A highly significant, positive correlation between Treml1 and neomycin expression was observed. Shown is the correlation from N = 18 animals ranging in neomycin expression. (Linear regression, R²=0.9879, P < 0.0001).