hey filled the dish. Then some of these cells were placed in a new dish until it was filled. The number of Areplatings@ necessary until the cells no longer grew and filled the dish represented the number of cell divisions (Ricklefs and Finch, 1995, 29). It is not known why the cells stop dividing, but these AHayflick limits@ may be caused by some genes responsible for halting the division of neurons during developmental stages (Ricklefs and Finch, 1995, 30). This limited number of cell divisions is often thought of as cellular aging (Lafferty et al., 1996, 55), a microcosm of the process of gradual, yet, actual deceleration and deterioration of the body. Though remarkable discoveries support the fact that cells stop dividing, this theory does not seem to recognize why cells stop dividing. Shortened Telomeres The theory that shortened telomeres are involved in aging is an extension of the cellular aging theory. Telomeres are highly repetitive sequences of nucleic bases found at the tips of chromosomes. They contain only a few genes. Their function is to protect chromosomes in a manner similar to Athe way a plastic cuff protects a shoelace@ (Lafferty et al., 1996, 57). After each DNA replication, telomeres on the daughter chromosomes become shorter than those on the parent strand. So after enough replications, which happens to be the Hayflick limit, the telomeres have become strikingly diminished and cell reproduction ceases. It has been theorized that at this point, genes previously protected by telomeres become revealed and produce proteins that aid in the deterioration of tissue, characteristic of the aging process (Lafferty et al., 1996, 57). To back up this theory, researchers have found that cells that do not stop dividing, such as sperm cells and many cancer cells, do not lose telomere DNA. These cells possess an enzyme called telomerase, which maintain telomeres (Lafferty et al., 1996, 57). If this is true, then with an extra boos...
