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. Author manuscript; available in PMC: 2009 Sep 15.
Published in final edited form as: Cell Cycle. 2008 Mar 10;7(9):1197–1204. doi: 10.4161/cc.7.9.5886

Figure 3.

Figure 3

The Clock mutation affects the level of radiation-induced apoptosis in radiation-sensitive lymphoid tissues. (A) Upregulation of several key proapoptotic and growth arrest-specific genes in the spleen of Clock/Clock mutant mice. Data presented as mean ± s.e.m., n = 18; *p < 0.001. WT—black bars, Clock/Clock— grey bars. mRNA expression levels were determined by real-time RT-PCR. Expression of the proproliferative gene Wee1 was significantly (p = 0.025) reduced in Clock mice. Consistent with previously reported data, spleens of Clock/Clock mice also showed significantly reduced levels of expression of direct transcriptional targets of the CLOCK protein, Dbp and Per2 (p = 0.002). (B) Percentage of viable (annexin V-negative) CD3- positive cells in thymuses of WT (black bars) and Clock/Clock (grey bars) mice at different times after 8.5 Gy of TBI. Data presented as mean ± s.e.m., n = 4, p = 0.005. (C) Percentage of viable (annexin V-negative) B220-positive cells in spleens of WT (black bars) and Clock/Clock (grey bars) mice after 8.5Gy of TBI. Data presented as mean ± s.e.m., n = 4, p = 0.05.