A telomere represents a region of recurring nucleotide chains at each end of the chromosome (Pierce, 2013). Telomeres serve three main purposes in a cell. First, they facilitate the organization of all 46 chromosomes in the cell nucleus. Second, they protect the ends of the chromosome from deterioration and fusion with neighboring chromosomes. Third, they guarantee proper replication of chromosomes during cell division.
Each time DNA replication occurs within the cell, chromosomes are shortened by about 25 – 200 bases per replication. The presence of telomeres at the ends of each chromosome ensures that the DNA is left intact during the replication process (Arai et al., 2015). Specifically, telomeres act as disposable buffers that get truncated instead of the genes on the chromosomes, a phenomenon that leads to the shortening of telomeres over time due to continuous cell division. To prevent the depletion of telomeres, the cell replenishes them with telomerase reverse transcriptase enzyme, which adds bases to their ends.
Telomerase enzyme is more active in young cells that require protection from excessive deterioration. Nevertheless, as cells divide over time, the amount of telomerase reduces significantly. This causes telomeres to grow shorter and the cells to age. Telomere shortening normally induces replicative senescence which impedes cell division. This mechanism prevents development of cancer and genomic instability by limiting the number of cell divisions. However, the shortening of telomeres can potentially damage the immune function and increase vulnerability to cancer (Eisenberg, 2011). Telomeres that experience excessive shortening usually unfold from their assumed structure, leading to limited cell growth.
Usually, cancerous cells divide more often than normal cells, meaning that telomeres become extremely shortened. Excessively shortened telomeres can lead to cell death. However, some cells escape death by producing more telomerase enzyme. Indeed, telomerase can make cells immortal. Doctors, can raise the lifespan of an individual by triggering sufficient amounts of telomerase in the human body (ScienceDaily, 2018). Nevertheless, telomerase increases the risks of cancer. If scientists learn how to stop telomerase in select situations, they may succeed in fighting cancer by making cancerous cells to age and die (Shay, 2002). Even so, there are a number of risks for blocking the enzyme as well, including impaired fertility, production of blood cells, and wound healing.
References
Arai, Y., Martin-Ruiz, C. M., Takayama, M., Abe, Y., Takebayashi, T., Koyasu, S., … & von Zglinicki, T. (2015). Inflammation, but not telomere length, predicts successful ageing at extreme old age: a longitudinal study of semi-supercentenarians. EBioMedicine, 2(10), 1549-1558.
Eisenberg, D. T. (2011). An evolutionary review of human telomere biology: the thrifty telomere hypothesis and notes on potential adaptive paternal effects. American Journal of Human Biology, 23(2), 149-167.
Pierce, B. A. (2013). Genetics essentials: Concepts and connections. WH Freeman.
ScienceDaily. (2018). Hidden secret of immortality enzyme telomerase: Can we stay young forever, or even recapture lost youth?. [online] Available at: https://www.sciencedaily.com/releases/2018/02/180227142114.htm [Accessed 29 Jun. 2018].Shay, J. W. (2002). Telomerase in cancer: diagnostic, prognostic, and therapeutic implications. Gaceta Médica de México, 138(S1), 4.
