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. 2007 Sep 19;104(39):15400–15405. doi: 10.1073/pnas.0706307104

Fig. 2.

Fig. 2.

Decreased apoptosis in mice deficient for E2f2 during tumorigenesis. (A) Development of double-negative thymocytes in 21-day-old E2f2+/+ (nontransgenic; white bars), E2f2−/− (nontransgenic; black bars), EμSR-tTA;Teto-MYC;E2f2+/+ (EμSR-tTA;Teto-MYC; white bars), EμSR-tTA;Teto-MYC;E2f2−/− (EμSR-tTA;Teto-MYC; black bars) as assessed by FACS. Staining with anti-CD4 and -CD8 antibody was used to determine CD4−CD8− double-negative population within the live lymphoid gate. Double-negative populations were subsequently analyzed for CD44 and CD25 surface expression. Data are presented as an average percentage ± SD for DN1 (CD44+), DN2 (CD44+CD25+), DN3 (CD44−CD25+), and DN4 (CD44−CD25−). (B) Graphic representation of tumor clonality in EμSR-tTA;Teto-MYC mice of the following genotypes: E2f2+/+, E2f2+/−, and E2f2−/−, as determined by analysis of different tissues using a panel of monoclonal antibodies recognizing different TCR Vβ chains. (C) BrdU incorporation and apoptosis assays of EμSR-tTA;Teto-MYC;E2f2+/+ (white bars) or EμSR-tTA;Teto-MYC;E2f2−/− (black bars) mice at final stages of disease as determined by FACS using anti-BrdU or anti-Annexin V antibodies. The number of mice used for each cohort is indicated by n. Student's t test was used for statistical analyses, and P values are shown.