It has been proposed that a decrease in the length of telomeres with the successive rounds of DNA replication that accompany mitotic division could play a causal role in the aging process. To investigate this possibility, telomeres from cells of the budding yeast Saccharomyces cerevisiae that varied in replicative age were examined. No change in the lengths of the telomeres was observed in cells that had completed up to 83% of the mean life span. We conclude that the length of the telomeres is not a contributing factor in the natural aging process in individual yeast cells.Eukaryotic chromosomes terminate in specialized structures called telomeres that serve a dual function. They stabilize the chromosome and sustain the ends of the chromosome by facilitating complete replication (34). Although the specific telomere sequence pattern is unique for an organism, the strand oriented 5' to 3' toward the end of the chromosome is always G rich. Experiments have shown that the telomere sequences obtained from diverse organisms, ranging from protozoans to humans, act as telomeres in yeast cells (3,7,25), suggesting that telomere function is highly conserved.Recent studies have elucidated the role of the repeats present in the telomere, and several models (2) have been proposed concerning the interaction of these repeats with telomerase, the enzyme that adds the repeating units to the telomeres. However, very little is known of the overall size and stability of telomeres during development and aging. We have examined the lengths of telomeres in aging yeast cells as part of our studies on the aging process of the budding yeast Saccharomyces cerevisiae.The life span of yeast cells is finite, since the cells exhibit a limited replicative capacity (22). The measure of the life span in yeast cells is not chronological age but the number of times the cell divides (23). Several of the characteristics that accompany aging in yeast cells reflect those exhibited by normal human diploid fibroblasts as they age in culture (14). Fibroblasts also display a finite replicative capacity and arrest at the G1/S boundary of the cell cycle when they reach the maximum population-doubling level (14). It has been proposed that shortening of telomeres occurs with successive rounds of DNA replication during somatic differentiation (6). Such shortening has been shown to occur in normal human diploid fibroblasts in culture as cumulative population-doubling levels increase (12). However, in vivo studies in mice, which exhibit hypervariable ultralong telomeres, have shown no significant shortening of telomeres during development and aging of the animal (15). In colorectal carcinomas, telomeres decrease in length on average compared with telomeres in normal colonic mucosa obtained from the same source (13). The change in telomere length, whether increase or decrease, appears clonal in nature. We undertook this study to ascertain whether telomeres shorten * Corresponding author.during the life span of a unicellular organism and whether such a change migh...
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