Scientists have come one step closer to answering how we age and how we develop cancer thanks to the collaborative efforts of Arizona State University scientists and the Chinese Academy of Sciences in Shanghai. Their findings give a first-ever look at the atomic level of telomeres, a genetic basis that has gained a reputation as the fountain of youth.

The research, which was published in the journal Nature Structural and Molecular Biology in April, highlights the importance of the ASU team’s discovery of the telomere’s role in our genetic makeup.

Telomeres are the caps at the end of chromosomes, often described as the plastic pieces on shoelaces because they keep the chromosomes ends from fraying apart and sticking to each other. They are responsible for cell division and many scientists believe they also hold the key to aging, and how cells can become cancerous.  Scientists find that when telomerase — an enzyme made of protein and RNA subunits that elongates chromosomes — is mutated, it is often the cause of human cancers and seems to make existing tumors grow faster.

"Telomerase is crucial for telomere maintenance and genome integrity," explains Julian Chen, professor of chemistry and biochemistry at ASU and one of the project's senior authors. "Mutations that disrupt telomerase function have been linked to numerous human diseases that arise from telomere shortening and genome instability."

Chen and her team have developed a way to purify the fragment function of the telomerase enzyme. Enzymes are crucial and complex biological proteins that cause specific chemical changes throughout the body. By being able to focus on a specific piece of the telomeres, scientists will be able to analyze and observe its function in the aging process.

Telomeres prevent chromosomes from breaking down by duplicating themselves during cell division, which preserves valuable genetic information. As the body ages, the telomeres’ length shortens throughout an individual’s life until it can no longer divide anymore, when it becomes inactive, and then dies. Those with shorter telomeres or telomerase mutations were more likely to experience an early death, or develop disease and neurodegenerative disorders.

In 2010, researchers at the Dana-Farber Cancer Institute and Harvard Medical School found that when there was in increase in telomerase, there was an increased chance of cancerous tumor growth. More importantly, when researchers removed the telomerase in mice they found the predictable signs of premature aging, however when the enzyme was replaced, they fully recovered their health. This offers the possibility that normal human aging could be slowed or eventually stopped all together.

The mysteries of the telomeres are slowly being unraveled; however scientists have a long way to go before they understand exactly how the enzyme functions.

Chen continues that, "Despite the strong medical applications, the mechanism for telomerase holoenzyme (the most important unit of the telomerase complex) assembly remains poorly understood. We are particularly excited about this research because it provides, for the first time, an atomic-level description of the protein-RNA interaction in the vertebrate telomerase complex."

Source: Chen J, Lei M, et al. Nature Structural and Molecular Biology. 2014.