Figure 3. A murine senescence reporter strain for gerontogenicity.

The recently published p16^LUC allele featuring firefly luciferase `knocked in' to the p16^INK4a promoter [29] was used to serially measure p16^INK4a expression in vivo with normal chronological aging (A) or after chronic exposure to cigarette smoke (B). In A, mouse age increases from left to right at ~15 week intervals from 18 to 96 weeks of age. In B, mice of the indicated genotypes are all of the same age with or without chronic (8 months) tobacco exposure [34]. Consistent with the fact the pulmonary exposure to tobacco smoke is poor using chamber inhalation models; note that the gerontogenic effects of cigarette smoking are anatomically localized to the nasal cavities and upper airways.