Figure 2.

Failure of transgenic Bcl-2 to normalize thymocyte cellularity in c-kit and γ_c single and double mutant mice in vivo. To asses the effect of transgenic Bcl-2 expression on thymus cellularity in growth factor receptor mutants, mice of eight different genotypes were generated: (A) wild-type mice without (c-kit⁺γ_c ⁺bcl⁻; ○) or with (c-kit⁺γ_c ⁺bcl⁺; •) the transgene; (B) mice deficient for γ_c without (c-kit⁺γ_c ⁻bcl⁻; □) or with (c-kit⁺γ_c ⁻bcl⁺; ▪) the transgene; (C) mice deficient for c-kit without (c-kit⁻γ_c ⁺bcl⁻; ▵) or with (c-kit⁻γ_c ⁺bcl⁺; ▴) the transgene; (D) mice deficient for both c-kit and γ_c without (c-kit⁻γ_c ⁻bcl⁻; ⋄) or with (c-kit⁻γ_c ⁻bcl⁺; ♦) the transgene. All mice were analyzed on postnatal day 5 because c-kit^W/W mice die by postnatal day 10. Numbers of mice per group are indicated above each group; below, the mean cell number ± 1 SD are shown. No significant differences were observed between bcl-2 transgenic and nontransgenic mice (Wilcoxon rank-sum test: A: transgenic vs. nontransgenic, rank-sum normal statistic with correction Z = −0.8997, P value = 0.3683; B: transgenic vs. nontransgenic, rank-sum normal statistic with correction Z = −1.645, P value = 0.1; C: transgenic vs. nontransgenic, rank-sum normal statistic with correction Z = −1.0839, P value = 0.2784, alternative hypothesis: true μ is not equal to 0; in D, no statistical comparison was done because thymocytes were undetectable in both groups of mice). Thymocytes were undetectable in c-kit⁻γ_c ⁻ mice regardless of the bcl-2 transgene.