Brca1 deficiency causes PB cytopenias, BM failure featuring genomic instability, and DNA crosslinking agent hypersensitivity. Complete blood counts from Brca1^+/+ (red), Brca1^+/− (green), and Brca1^−/− (blue) mice were measured once per month up to 6 months of age. (A) Hb concentration (g/dL); (B) mean corpuscular volume (MCV) (fL). The number of mice in each cohort at each time point analyzed is listed in supplemental Figure 2. Analysis of variance was used to analyze for differences in counts at each time point (*P < .01). PB smears from (C) a Brca1^+/+ (7145) and (D) a Brca1^−/− (7386) mouse are shown (magnification ×10). BM sections from (E) a Brca1^+/+ (7145) and (F) a Brca1^−/− (7386) mouse are shown (magnification ×10). (G-H) Spectral karyotyping analysis revealed multiple structural abnormalities, including chromatid exchanges and premature centromere divisions. Representative cell karyotype in G: 40,XX,chte(2;5)(F1;C2),chte(9;12)(F1;E),pcd(16)(A)[1]. (I) Representative fluorescence-activated cell sorter plots from spleen cells from a Brca1^+/+ (B7292) and a Brca1^−/− (B7386) mouse stained with antibodies against CD71 and Ter119. (J) Average proportion of spleen cells accumulating in regions I, II, III, and IV of red blood cell differentiation after staining with antibodies against CD71 and Ter119. Student t test was used to analyze the differences in the proportion of cells within each region. (K) Sensitivity of Brca1^−/− cells (blue) relative to Brca1^+/+ cells (red) in methylcellulose colony-forming assays to mitomycin C at doses of 0, 5, 10, 25, and 50 nM. Averages are shown with standard error of the mean. chrb, chromosome break; chrg, chromosome gap; chtb, chromatid break; chte, chromatid exchange; chtg, chromatid gap; pcd, premature centromere division.