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. Author manuscript; available in PMC: 2013 Apr 15.
Published in final edited form as: Science. 2010 Oct 15;330(6002):379–385. doi: 10.1126/science.1195262

Figure 5. Inhibiting HSF-mediated transcription lengthens circadian period and impairs temperature compensation.

Figure 5

(A) SCN in KNK437 where marked by an orange line. Numbers indicate the period of the rhythm underneath the line. (B) Periods of SCN in KNK437 (orange) at 100 μM (n=5), 30 μM (n=5), 10 μM (n=5), 3 μM (n=5), and 1 μM (n=5) displayed as mean +/− SEM. Gray points indicate the periods of the same SCN cultures after KNK437 was removed. * indicates p < 0.05 from paired t-tests corrected for multiple measures. (C) Traces of bioluminescence from pituitary or lung cultured with DMSO (black/gray) or 100 μM KNK437 (orange/red). (D) Periods (mean +/− SEM) of SCN or pituitary in 100 μM KNK437 or DMSO. SCN: 30°C DMSO n=8, KNK n=5, and TTX n=; 36°C DMSO n=9, KNK n=8, and TTX n=8; 38°C DMSO n=8 and KNK n=8. Pituitary: 30°C DMSO n=6 and KNK n=6; 36°C DMSO n=9 and KNK n=7; 38°C DMSO n=7 and KNK n=8. p < 0.05 comparing drug treatment or temperature within KNK groups (ANOVA); N.S. for temperature in vehicle groups (ANOVA). (E) Model representing the communication between dorsal and ventral SCN which confers phase resistance to body temperature changes which are regulated by the SCN. Body temperature then entrains peripheral oscillators by acting through HSF mediated transcription.