Osteopetrosis and thalamic hypomyelinosis with synaptic degeneration in DAP12-deficient mice
J. Clin. Invest. Tomonori Kaifu, et al. 111:323 doi:10.1172/JCI16923 [Go to this article.]

Figure 1
Targeted mutation of the DAP12 gene in mice. (a) Schematic illustration of the DAP12 locus (top), targeting vector (middle), and disrupted allele (bottom). Exons 1–5 (I–V) are shown (filled boxes). Exon 4 of the DAP10 gene is also shown (open box). The neo^r (neo) and thymidine kinase (TK) genes and the probe (shaded box) for Southern blotting are shown. A 5.1-kb BamHI fragment containing the promoter region and exons 1–3 of the DAP12 gene was replaced by a neo^r cassette; 5.1 kb and 1.2 kb of homologous sequences flanking the neo^r cassette were retained. (b) Southern blot analysis to confirm the genotype of DAP12 wild-type (+/+), heterozygote (+/–), and knockout (–/–) offspring. Genomic DNA isolated from the tail tips of offspring of heterozygous intercrosses were digested with KpnI and probed. The wild-type allele migrates as a 6.0-kb fragment; the disrupted allele, 4.8 kb. (c) Immunoblot analysis. Protein extracts from IL-2–induced LAK cells (5 × 10⁵ cell equivalent per lane) of wild-type or DAP12^–/– mice were probed with rabbit anti-DAP12 antiserum (1:1,000 dilution) or β-actin antibody. DAP12 protein was not detected in the cells from DAP12^–/– mice.