Extended Data Fig. 3: Targeting vector, BAM targeting selectivity, and efficiency of ApoE deletion in Mrc1^Cre+ mice crossed with R26^tdT, ApoE3^fl/fl, or ApoE4^fl/fl mice.

a. DNA construct used to generate Mrc1^Cre+ mice. Tamoxifen (TAM) treatment of Mrc1^Cre+/R26^tdT crosses induces recombinase activity in over 80–90% of cells expressing the BAM marker CD206 but not in Iba1⁺ microglia or CD31⁺ cerebral endothelial cells. N = 5 mice/group; represented images selected from N = 5 mice/group; 2-3 sections analyzed in neocortex per mouse; unpaired t-test; mean±SEM. b–e. Dual RNAScope in situ hybridization with mRNA probes for Mrc1 (green) and ApoE (magenta), combined with DAPI nuclear staining (blue) and the basement membrane marker laminin (yellow). Representative images showing expression of ApoE in Mrc1⁺ cells in Mrc1^Cre+/ApoE4^fl/fl (b) and Mrc1^Cre+/ApoE3^fl/fl (c) mice treated with vehicle (corn oil). However, in Mrc1^Cre+/ApoE4^fl/fl (d) and Mrc1^Cre+/ApoE3^fl/fl (e) mice treated with TAM ApoE levels in Mrc1⁺ cells are markedly reduced. Scale bars = 20 µm in a–e. f–g. The number of Mrc1⁺ cells (f) and their Mrc1 puncta (g) is comparable in vehicle- and TAM-treated Mrc1^Cre+/ApoE4^fl/fl and Mrc1^Cre+/ApoE3^fl/fl mice. N = 5 mice/group; 1-2 sections/mouse; 5–12 cells analyzed in neocortex per section; two-way ANOVA with Tukey’s test; mean±SEM.

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