How do your cells know what time it is?   Answer:  Telomeres

First, what is a telomere:

Telomeres are sequences at the ends of chromosomes. Though they are written in the 'alphabet' of the genes, telomeres do not contain the codes for proteins. So telomeres are not themselves genes, but neither are they meaningless junk. Instead these repetitive sequences protect the ends of the chromosome from damage, and prevent the chromosomes from fusing into rings, or binding haphazardly to other DNA in the cell nucleus.

When a cell divides, the chromosomes are copied by enzyme molecules. These molecules faithfully transcribe the genetic information on each chromosome, producing mirror images of both of the two original strands (which themselves were mirror images of each other). But the enzyme molecules that do the duplicating are unable to completely reproduce the tips of the chromosomes, much as a tape recorder can not play the last few centimeters of tape in a cassette. As a result, the duplicate chromosome is necessarily slightly shorter than the original, lacking a small amount of the original telomere sequence. The missing DNA does not measurably affect cellular functioning until enough cell divisions have occurred that the telomeres on at least one of the chromosomes in the cell become critically short.
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Cells with critically short telomeres alter their character by transcribing a partly distinct set of genes. They also become unresponsive to triggers that would normally stimulate them to divide. Though these growth arrested cells can live on in the body for years, once they have reached this state, they do t under normal circumstances, replicate themselves. They are said to have reached their Hayflick limit (named for the discoverer of the arrested state).

Telemerase:

there are a number of mechanisms in nature that counteract the natural tendency of telomeres to erode over time. Vertebrates, including mammals, use a remarkable enzyme dubbed 'telomerase'. This hybrid molecule, part protein, part RNA, is capable of slowing telomere erosion, halting erosion altogether, or lengthening telomeres beyond those in the parent cell. The genes that produce telomerase are found in every potentially replicating cell in the body
Source: 

http://www.telomere.net

Sensence:

Though the connection is still controversial, many biologists believe that the senescent decline observed in mammals is the result of an ever increasing percentage of cells across the body reaching their Hayflick limits. Clearly, if an ever larger percentage of the body's cells are unable to reproduce, then defense, maintenance and repair of the body would become increasingly difficult tasks. Thus, telomere erosion and Hayflick limits could account for most of the decline in efficiency, and increases in vulnerability that characterizes the aging of sexually mature mammals.

The evidence supporting this perspective has grown substantially in the last few years of research. Further, the discovery that several diseases that produce syndromes of apparently accelerated aging in humans (e.g. Hutchinson-Gilford progeria and Werner's syndrome) have now been linked to telomere-system defects, strongly suggest that this mechanism is fundamental to the explanation of aging in humans

http://www.telomere.net

Sensence:

Though the connection is still controversial, many biologists believe that the senescent decline observed in mammals is the result of an ever increasing percentage of cells across the body reaching their Hayflick limits. Clearly, if an ever larger percentage of the body's cells are unable to reproduce, then defense, maintenance and repair of the body would become increasingly difficult tasks. Thus, telomere erosion and Hayflick limits could account for most of the decline in efficiency, and increases in vulnerability that characterizes the aging of sexually mature mammals.

The evidence supporting this perspective has grown substantially in the last few years of research. Further, the discovery that several diseases that produce syndromes of apparently accelerated aging in humans (e.g. Hutchinson-Gilford progeria and Werner's syndrome) have now been linked to telomere-system defects, strongly suggest that this mechanism is fundamental to the explanation of aging in humans

http://www.telomere.net

Sensence:

Though the connection is still controversial, many biologists believe that the senescent decline observed in mammals is the result of an ever increasing percentage of cells across the body reaching their Hayflick limits. Clearly, if an ever larger percentage of the body's cells are unable to reproduce, then defense, maintenance and repair of the body would become increasingly difficult tasks. Thus, telomere erosion and Hayflick limits could account for most of the decline in efficiency, and increases in vulnerability that characterizes the aging of sexually mature mammals.

The evidence supporting this perspective has grown substantially in the last few years of research. Further, the discovery that several diseases that produce syndromes of apparently accelerated aging in humans (e.g. Hutchinson-Gilford progeria and Werner's syndrome) have now been linked to telomere-system defects, strongly suggest that this mechanism is fundamental to the explanation of aging in humans