Similar to our control experiments (Fig. 1), group mean activity profiles from Bmal1+/+ mice showed that mice were active during the time of prior food availability on the first (601±1005) and second (4104±1941) days of food deprivation (Fig. 2B; FAA from individual mice shown in Fig. 3B).
Although the details of timed gene expression are likely to differ between mice and humans — mice are active at night rather than during the day — it could be that the majority of human genes fall into this category.
Others were given access to running wheels only in the early portion of their waking time (mice are active at night) or in the later stages, the equivalent of the afternoon for us.
The LysM gene in mice is active mostly in monocyte/macrophages and neutrophils [38], [39].
In the social interaction test in the home cage, time spent separated is usually increased when mice are active and decreased when mice are sleeping.
It is intriguing that hypothalamic AMPK activity has a diurnal oscillation that peaks during the dark period when mice are active and eating.
The CD2 promoter used to create Egr-2 cKO and cTg mice is active in both T and B lymphocytes [17].
In contrast, by gradually reducing food availability and by placing food pellets on the bottom of the cage, we found that most Bmal1−/− mice were active and healthy during restricted feeding [39].
Both WT and Bst+/− mice are active in the light and inactive in the dark, suggesting that circadian rhythm physiology is preserved in the Bst+/− mouse (Fig. 2B).
