Circadian clock is implicated in the regulation of aging. The transcription 
factor CLOCK, a core component of the circadian system, operates in complex with 
another circadian clock protein BMAL1. Recently it was demonstrated that BMAL1 
deficiency results in premature aging in mice. Here we investigate the aging of 
mice deficient for CLOCK protein. Deficiency of the CLOCK protein significantly 
affects longevity: the average lifespan of Clock-/- mice is reduced by 15% 
compared with wild type mice, while maximum lifespan is reduced by more than 
20%. CLOCK deficiency also results in the development of two age-specific 
pathologies in these mice, cataracts and dermatitis, at a much higher rate than 
in wild type mice. In contrast to BMAL1 deficient animals, Clock-/- mice do not 
develop a premature aging phenotype and do not develop the multiple 
age-associated pathologies characteristic of BMAL1 deficiency. Thus, although 
CLOCK and BMAL1 form a transcriptional complex, the physiological result of 
their deficiency is different. Our results suggest that CLOCK plays an important 
role in aging, specifically; CLOCK activity is critical for the regulation of 
normal physiology and aging of the lens and skin.