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Mutants were bred and genotyped as described for each mutant [26], [27].
Balb/c, CBA and C57 Black/6 mice were obtained from Charles River (UK) and Mc1r e/e and Mc3r KO mutants were bred in-house.
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Surviving Vangl2 Lp /+; Scrib Crc /+ double-mutant males were bred with Celsr1 Crsh /+ females to generate triple-mutant embryos.
The mutant mice were bred in the 129sv/C57BL6 genetic background.
Mutant lines were bred for two generations to minimize any off-target effects from the genome editing, and we studied the F3 generation for cardiac and skeletal muscle consequences.> -wrap-foot> As expected (Xu et al., 2002; Gramlich et al., 2015), ttna truncations showed no gross phenotype in heterozygotes, with all heterozygotes attaining sexual maturity.
Male mutants from this line were bred to females of different genetic background including 129S1, FVB inbred lines and CF1 outbred mice.
When cox-2 null mice were bred with ApcΔ716 mutant mice, tumor burden in the offspring decreased in a gene dose-dependent fashion (Oshima et al., 1996).
Tg2576 mice, expressing the Swedish mutant form of APP (APP K670N, M671L) [15], were bred into Irs2 −/− mice [16] as follows: male Tg2576 (C57Bl/6.SJL) were initially crossed with Irs2 +/− females (C57Bl/6).
To visualize individual fibers, the sparse-labeling alleles were bred onto the Sema3f mutant line.
Wild type (WT), Mavs−/−, Myd88−/−, Myd88−/−Mavs−/−, Unc93b1 mutant (3d), TLR2−/−TLR4−/− and TLR7−/− mice were bred and maintained under specific pathogen-free conditions in the animal care facility of University of Texas Southwestern Medical Center at Dallas.
Mutant strains that showed a 7-day memory deficit in the primary screen (and their controls) were bred according to the Jackson Laboratories protocol for each mutant strain.
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