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Possible Connection Between Transposons and Aging


Research on the processes and causes of aging has existed for thousands of years, motivated by the hope that a true understanding of the aging process could lead to slowing, or perhaps even halting, it entirely. While some biogerontologists still pursue this goal, the majority of the scientific community currently focuses less on the possibility of immortality, and more on simply understanding the complex process of aging – a concept which, despite many years of research, remains mysterious.

Modern biologists generally break into two schools of thought regarding aging: the free radicals theory and the DNA damage theory. Proponents of the free radicals theory emphasize the damage caused by oxidative stress on molecules. These highly-reactive molecules cause an effect similar to that of rusting within the body, and this concept leads many to promote foods with high antioxidants as a way to delay aging. The DNA damage theory focuses on breakdowns that occur in the genetic code. One focus of this theory is the gradual shortening of telomeres during an individual’s lifetime. Telomeres, which are specialized structures on the ends of chromosomes, are comprised of repeating DNA base pairs (‘TTAGGG’ in humans) that protect functional portions of the DNA strand from damage during the replication process. Since replication has occurred many more times in older individuals, more and more of the telomeres have been eaten away by the process, and shorter telomeres can lead to DNA damage, which may, in turn, lead to cell death or cancer.

It is also quite possible that the aging involves free radicals and DNA damage both, as well as many other processes. One of these additional processes within the theory of DNA damage is the potential role of transposable elements. Transposable elements are segments of DNA that have mobility within the genome. Using a process of recombination, these segments of DNA replicate themselves and move along the DNA strand, reentering in random target locations. If the target location happens to be in the middle of a functional gene, the insertion of the transposon would disrupt the gene and prohibit it from displaying any associated phenotype.

This mobile DNA causes increased genetic variety, but as one might imagine, it can also cause several problems if the wrong genes are disrupted. The list of human diseases that are known to be caused by transposons is quite long and includes breast cancer, colon cancer, and leukemia. What connects this to aging is that transposons replicate each time DNA replicates. In theory, this makes it more likely for more transposable elements to interrupt genes that are responsible for hair color, or whose interruption might cause cancer or disease later in life. For this reason, transposons can be considered genome parasites, since their sole function appears to be replicating themselves (Craig 2010).

The idea of a possible link between transposons and aging is not new. Studies have been performed on the concept since the early 1990s, especially in species of Drosophila (Driver 1992). Modern studies with these same model species have shown that there is an increased number of transposons in the neural cells of aged flies, and that mutations resulting in exacerbated transposon activity caused a shortened life span and reduction in age-dependent memory (Li, 2013). While the aging processes in fruit flies may not necessarily be similar to those of humans, transposons have been shown to become more mobile and active in aging mammalian tissue (De Cecco 2013). An additional 2015 research paper (Sturm 2015) reveals evidence that in areas of the genome that do not exhibit aging or mortality, (such as germ-line cells in most organisms, and somatic cells in an organism known as the Hydra, which is believed to be functionally immortal,) transposable elements are functionally silenced by a Piwi-piRNA pathway. This seems to be the difference between the somatic and germ-line’s differences in aging.

The idea that transposons exist in the genome without cause or purpose seems a bit simplistic, as their conservation across all three kingdoms of life suggests their necessity. Researchers are even beginning to find some necessary functions in ‘junk’ DNA, which was previously thought to be useless, and transposons’ base sequencing is much more complex than that of junk DNA. While aging may not seem like a beneficial evolutionary advancement, species in which individuals do not die could quickly exceed their carrying capacities and face extinction. Death could actually be necessary for species advancement, so the reason that all species have transposable elements could be that aging is necessary for species’ survival.

The truth is that many questions remain about the aging process, and that the link between transposons and aging is far from concrete. The Scientific Student reached out to aging expert Joao Pedro de Magalhaes of the University of Liverpool, and his concerns on transposon theory matched those of several other top scientists. While correlations have been shown in the studies cited and others, it is very difficult to prove any causational relationship in the aging process.

Interested or involved in aging research? Comment below your opinions on transposons, the Piwi-piRNA pathway or any other possible aging processes.

De Cecco, Marco, et al. 2013. “Transposable elements become active and mobile in the genomes of aging mammalian somatic tissues.” Aging 5.12: 867-883.

Driver, Christopher JI, and Stephen W. McKechnie. 1992. “Transposable elements as a factor in the aging of Drosophila melanogaster.” Annals of the New York Academy of Sciences 673.1: 83-91.

Li, Wanhe, et al. 2013. “Activation of transposable elements during aging and neuronal decline in Drosophila.” Nature neuroscience 16.5: 529-531.

Sturm, Adám, Zoltán Ivics, and Tibor Vellai. 2015. “The mechanism of ageing: primary role of transposable elements in genome disintegration.” Cellular and Molecular Life Sciences 72.10: 1839-1847.

Edited by: Rachel Levy, Daryn Dever, and Naomi D’Arbell