Deoxyribonucleic acid, more commonly referred to as DNA, acts as the blueprint for life – it houses all the instructions needed for us to function. It’s this DNA that micromanages the millions of cellular reactions that take place inside our cells every second, and it’s the very reason you’re able to read this article. As such, our DNA is our most prized possession, and we do everything we can to protect it – from enveloping it with layer upon layer of membranes for protection, to keeping it locked inside one designated location in the cell – the nucleus.
Our cells need to divide and reproduce in order to survive, grow and repair damaged tissues in the body. Each cell in our body requires this prized set of DNA to allow it to carry out its functions, and so DNA must also be copied into these new cells to allow them to function.
If we bring this situation into a real world context, we can imagine the cells of our body as employees, all working for the company known as ‘the human body.’ The DNA acts as an instruction set, which the employees must follow in order to complete their work. For every new cell made (or every new employee hired), this instruction set must be copied and given to them before the start of their job, to ensure that they don’t make any mistakes.
Yet here is where the problem lies – the DNA is shortened every time it is copied to be used in a new cell. Essentially, our instruction set loses its last few pages every time it is copied to be given to a new employee. This is a huge problem, and this loss of DNA could have catastrophic consequences.
In order to prevent this loss of instructions, our DNA is protected by a battalion of fearsome soldiers called telomeres, who give up their lives to protect our DNA. There is no way to stop DNA from being shortened every time it is copied, so we have special nucleotides (known as telomeres) present at the end of our DNA strands, which take the hit for our DNA and sacrifice themselves when DNA is copied, to prevent us from losing this instruction set which is so vital to life. 
Yet even this valiant army of soldiers is destined to fall eventually, and after around the 60th cell division, the soldiers are overwhelmed. Once the cell reaches this stage, it is said to enter a stage called ‘senescence’, where it is unable to divide and copy its instructions any further, so as to prevent any loss of DNA. 
But if cells are unable to reproduce past a set number of divisions, how do we grow all the time? There are certain cells in the body which act as an exception to this rule, which many of you may know as stem cells.
So what makes these cells so special? We can think of stem cells as having special doctors present called telomerases, which are able to heal the wounds of our injured soldiers, and allow them to once again stand in front of the DNA and be shortened instead. 
In reality, telomerase is an enzyme which is able to recreate telomeres on the end of the DNA strands once again, and this cycle of losing telomeres and building them back up repeats again and again over many cell divisions, allowing the cell to divide continuously.
Telomerase is a really fascinating enzyme, and in reality, it is much more complex than I’ve described. It has a very different structure to most enzymes (namely the addition of another substance known as RNA).
Here we see yet another example of nature’s age old paradox: the link between form and function, as telomerase would not be able to play the vital role it does without these key structural changes. 
A lot of research is being conducted into telomeres and the key role they play in protecting our DNA. Many links have been made between telomeres and the process of aging, and it is thought that telomeres are a more realistic indicator of our true biological age than the societal construct of chronological age. The presence of shortened telomeres has also been linked to an increased incidence and earlier onset of diseases, and it has also been noted that the rate of telomere shortening may be influenced by lifestyle factors, such as smoking. 
- Moof University (2013) “Telomeres and telomerase in eukaryotes” https://www.youtube.com/watch?v=28jwKIvsL90
- Khan Academy (2015) “Telomeres and cell senescence” https://www.youtube.com/watch?v=R5YiO6rKr-w
- Biomedical and Biological Sciences (2016) “A full explanation about the Telomerase and the end replication problem” https://www.youtube.com/watch?v=ohm-avnDYcM
- Masood A. Shammas (2011) “Telomeres, lifestyle, cancer and aging” Last accessed: 14 January 2011: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370421/