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. Author manuscript; available in PMC: 2013 Aug 28.
Published in final edited form as: Cell. 2013 Feb 28;152(5):1091–1105. doi: 10.1016/j.cell.2013.01.055

Figure 2. The Psttm mutation shortens period and antagonizes the period lengthening effect of the Ovtm mutation in FBXL3.

Figure 2

A. Representative actogram of tetO::Psttm #11 single transgenic mouse (left). Representative actogram of tetO::Psttm #11 transgenic mouse with the Scg2::tTA driver (right). Arrowheads indicate LD to DD transition. Doxycycline-containing (10 μg/ml) water was administered during the interval indicated by yellow shading on the actogram.

B. Free-running periods of single and double transgenic mice during constant darkness with water (black), Dox (yellow), and water after Dox treatment (grey). Error bars show SEM (tetO::Psttm #11 n = 3, Scg2::tTA/tetO::Psttm #11 n=5; *p < 0.05, Bonferroni corrected pair-wise comparison).

C. Representative PER2::LUC bioluminescence recording of SCN and pituitary explants from WT and homozygous Psttm mice. Blue and red traces represent PER2 rhythm from WT and Psttm mice, respectively. WT SCN mean circadian period: 24.76 hr (n=6), Psttm SCN mean circadian period: 23.36 hr (n=6). t test: *p-value 0.0027. WT pituitary mean circadian period: 23.2hr, N=6; Psttm pituitary mean circadian period: 22.61hr, N=6. t test: **p-value 0.0004.

D. Representative actograms of WT, Ovtm/Ovtm, Psttm/Psttm and Ovtm/Ovtm Psttm/Psttm mice subjected to the same experimental schedule as in Fig. 1B.

E. Period distribution. The four panels from top to bottom represent WT, Ovtm/Ovtm, Psstm/Psstm and Ovtm/Ovtm Psttm/Psttm mice, respectively. ANOVA of the period was performed among the genotype groups. Results: DF = 3; F= 388.507; p = 2.295 × 10−51. See also Figure S2 and Table S1.