p53 mediates the developmental abnormalities and impaired lymphocyte differentiation in the Mysm1^−/− mice. Data from mice of the following genotypes is presented: Mysm1^+/−p53^+/+, Mysm1^+/−p53^−/−, Mysm1^−/−p53^−/−, and Mysm1^−/−p53^+/+. Mysm1^+/− mice were shown to be phenotypically indistinguishable from wild-type throughout our previous studies, and in this case the comparison against Mysm1^+/− allowed the experimental mice to be bred as age-matched littermates. (A) Representative photograph of the mice, showing that loss of p53 rescues the growth retardation, as well as the tail and hind-limb abnormalities of the Mysm1^−/− mice. (B) Mouse lengths and weights. (C) Representative flow cytometry plots of mouse bone marrow, stained for B220 and CD19, and gated on live cells. Average percentage of cells within the B220⁺CD19⁺ B-cell lineage gate is shown. (D) Representative flow cytometry plots of the mouse spleen, stained for B220 and CD4, and gated on live cells. Average percentages of cells within the B220⁺ B-cell gate and CD4⁺ T-helper cell gate are shown. (E) Numbers of B- and T-lineage cells in the spleen of the mice; cells gated as B220⁺, CD4⁺, or CD8⁺. (F) Numbers of pro-B and pre-B cells (B220⁺IgM⁻IgD⁻), immature B cells (B220⁺IgM⁺IgD⁻), and mature B cells (B220⁺IgM⁺IgD⁺) in the bone marrow of the mice. (G) Numbers of double-negative (CD4⁻CD8⁻), double-positive (CD4⁺CD8⁺), and CD4 and CD8 single-positive thymocytes in the mice. Bars show means ± SEM; *P < .05, **P < .01, ***P < .001; all data are from 4 to 5 mice per group, and are representative of 3 independent experiments. NS, nonsignificant using analysis of variance with the Bonferroni post-hoc test; SEM, standard error of the mean.