Since the dawn of time, scientists have searched for ways to slow the rate at which we age. Science-fiction novels and movie adaptations have all tackled this seemingly unimaginable reality in a variety of ways through time travel and cryosleep (deep freezing bodies to revive in the future). More recently, a scientific breakthrough claims that the solution to this age-old question may lay right in our DNA: telomeres.
Telomeres sit at the tips of our chromosomes and are often compared to aglets on shoelaces; they prevent the unravelling of fabric, or in this case, our DNA[1]. They play a crucial role in preserving the information in our genomes[2]. Every time our cells divide, a small portion of DNA is lost, however, telomeres exist to prevent this from happening on a larger scale. Since telomeres are made up of the same six nucleotides (the building blocks of DNA) repeated over and over, this makes them somewhat disposable[1]. As a result, they are able to protect the rest of the DNA by gradually shortening without the loss of any important genetic information[2].
A factor that determines the lifespan of a cell or an organism is telomere length. With each DNA replication, telomeres gradually shorten until they reach a “critical point” at which they can no longer divide[1]. The cell becomes inactive and undergoes apoptosis, or controlled cell death, as it slowly accumulates damage that it can not repair. This cell division limit, “Hayflick Limit”, is named after researcher Leonard Hayflick who, in 1961, discovered that normal cells divide 50 times before stopping[3].
At the time of his discovery, it was still widely believed that cells were to divide infinitely given the appropriate conditions. Hayflick, young and ambitious, carried out a series of experiments that proved this theory false[3]. He compared two types of human fibroblasts (connective tissues that heal wounds): males ones that had divided many times with female ones that had only divided a few times. His observations imply two theories that both support the existence of a cellular counting mechanism: “first, that … cells only undergo a specific number of [replications], and second, that … preserved cells can ‘remember’ how many times they have divided”[3].
Fast forward to 1978, molecular biologist and Nobel Prize winner Elizabeth Blackburn founded the nucleotide sequence in telomeres, in mammals, to be TTAGGG, which allows for the length of telomeres to be measured[3]. Moreover, a challenge that researchers face is that telomere lengths are generally measured in the blood[4]. This fails to give a full picture of telomeres within the whole body since their lengths differ from other organs and tissues[3]. Since the correlation between telomere length and one’s health has only been recently discovered, it is still too early to tell exactly how dependent they are on one another[4].
Blackburn is also credited with the discovery of telomerase, an enzyme that elongates telomeres (nature). This enzyme exists within germline cells (egg and sperm cells) so that the telomeres in these cells do not shorten. However, somatic cells, which are all other cells apart from the reproductive ones, have low levels of this activity so their telomeres continue to undergo a progressive shortening[2]. As a part of the natural cell replication cycle, a too-short telomere is able to flag a problem within the DNA to promptly stop its replication cycle so it can be quickly repaired. This process may also be applied to prevent cancer, though we are unable to extend the length of telomeres because it would interfere with the body’s natural cancer prevention systems[1].
In addition to telomere length, their shape and structure equally matter too. In healthy telomeres, there should be “neat little paper-clip shaped loops at the ends of chromosomes”[1]. These serve to protect the DNA by keeping the important genetic information tucked away[2]. An analogy for this would be: as a piece of string gets shorter, it becomes harder to form a loop or knot; the same being true to telomere length[1]. In the case that the loop does come undone and the end is exposed, the cell’s telomeres will signal that the DNA is broken. Cell division will come to a halt, and the cell may become inactive, unable to repair itself, leading to its slow deterioration that we call the ageing process[1].
Although scientists have yet to fully understand whether telomeres are a direct cause of aging, it is safe to say that lifestyle choices can speed up their degradation[4]. This means that it is important to adopt healthy habits to ensure that we slow down that process and live a long and plentiful life.
References
[1]Graves, A. What are telomeres? Australian Academy of Science. https://www.science.org.au/curious/people-medicine/what-are-telomeres
[2]Shammas, M., A. (2011). Telomeres, lifestyle, cancer, and aging. Curr Opin Clin Nutr Metab Care. 2011 Jan; 14(1): 28–34. doi: 10.1097/MCO.0b013e32834121b1
[3]Shay, J., Wright, W. (2000). Hayflick, his limit, and cellular ageing. Nat Rev Mol Cell Biol 1, 72–76. doi: 10.1038/35036093
[4]Weintraub, K. (2017). You may have more control over aging than you think, say ‘The Telomere Effect’ authors. STAT. https://www.statnews.com/2017/01/03/aging-control-telomere-effect/
Written by Lananh Vo
Edited by Rachel Glantzberg
Graphics by Samantha Gu
Group advised by Ruhi Sahu
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