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While scrolling on the internet, it is not uncommon to come across the statement that lobsters are biologically immortal. This dubious fact was a popular meme in some internet circles a few years ago; however, as with many viral trends, those brief, digestible quips did not capture the whole picture. By returning to the curious case of the lobster, this article explores why the lobster is theoretically but not functionally biologically immortal.
The basis of all life, DNA, also known as deoxyribonucleic acid, is crucial to understanding the physiology of the lobster. DNA is solely responsible for the burden of maintaining life. The DNA of all living organisms essentially functions as a database of instructions for important cellular components known as proteins. These proteins take up a wide range of biological functions, from facilitating chemical reactions within cells to serving as the functional units of muscles. Even if all other cellular machinery were to remain intact, there would be no way to make the proteins needed to function without instructions from our DNA.
Because DNA is crucial to the functioning of every cell, it must be replicated every time a cell divides. Otherwise, at least one of the cells that remain after division wouldn't have the complete genetic code they need to survive. In simplified terms, DNA replication proceeds as follows:
First, an enzyme known as helicase "unzips" the two strands that make up the DNA molecule by breaking through the hydrogen bonds that connect the fundamental units called nucleotides. This allows both "halves" of the molecule's trademark double-helix shape to be replicated. Certain proteins, called Single-Stranded Binding Proteins (SSBPs) help keep the two strands from re-attaching to one another once they are separated. Another enzyme, topoisomerase, prevents the DNA ahead of helicase from getting too tightly wound.
Next, an enzyme known as primase sets down a small piece of RNA. RNA, or ribonucleic acid, is DNA’s sister molecule that also carries messages using nucleotides. This piece of RNA is known as a primer. The primer is what allows the DNA-building enzyme, DNA polymerase, to attach new nucleotides to each strand. DNA polymerase can only add nucleotides in a single direction, and it needs to build off of the small RNA primer supplied by primase. DNA polymerase adds nucleotides to both strands of DNA to create new complements for each one. The two strands of DNA wind in opposite directions from one another in an antiparallel way; nucleotides can only be added in a particular direction due to the chemical makeup of DNA. One "half" of the original DNA molecule has new bases added constantly as helicase "unzips" the DNA and the other half is built in small fragments from multiple primers laid into the constantly unwinding DNA. Finally, an enzyme known as ligase connects any disconnected fragments together to form cohesive replicated strands of DNA.
While this process seems perfected, there is one quirk in the system that results in DNA molecules shortening every time they are replicated. Primers are required to kickstart the replication process; however, because they are made of RNA, they are not assimilated into the final replicated strands. The nucleotides they bound themselves to are blocked from receiving complement nucleotides from DNA polymerase. This means that the newly-made strands are inevitably a few nucleotides shorter than the ones they were based on. Over many generations of replication, this results in a significant shortening of DNA which eventually impacts one’s lifespan and mortality.
However, every piece of DNA is capped off with a series of "junk" messages called a telomere that do not code for anything. Therefore, cell function is not impacted when telomeres are shortened. Nevertheless, these buffers, too, are finite. Outside of certain cells and certain types of cancer cells, telomeres are never repaired and gradually get shorter with each new generation of cells. Eventually, cells run out of telomeres to shorten, and they stop reproducing. The shortening of these finite buffers has been linked with the phenomenon of senescence, the biological changes related to growing old. While telomeres are likely only one part of aging, shortened telomeres in certain cells have been positively correlated to the incidence of diseases experienced toward the end of life, as well as an overall higher rate of death.
Most cells in lobsters have their telomeres repaired all throughout their life. A certain enzyme known as telomerase replaces the bases that are lost each time DNA replicates, preventing DNA from getting shorter through replication. As a result, lobsters never experience classical signs of senescence. They don't experience a decrease in fertility or strength as humans and other animals do as they get older. Their cells never hit a limit where they cease to divide. If there were no other forces at play in a lobster's lifespan, this would be enough to grant them the title of biological immortality. However, unfortunately for the lobster, their cells are only theoretically immortal.
Unlike many animals, lobsters continue to grow throughout their entire lifespan. For these exoskeleton-wearing crustaceans, this means that they must molt their shells regularly to keep up with their increasing size. Molting is a very vulnerable and demanding process, which alone may be responsible for 10-15% of lobster mortality. The larger a lobster grows, the more energy is required to successfully molt. At a certain age and size, it becomes physically impossible for a lobster to supply the energy required to molt further. At that point, the lobster will die, not of classical old age, but of exhaustion. They quite literally get too big for their britches and fall just short of being biologically immortal because of it.
The nature of a lobster’s life poses the question of whether humankind can utilize telomerase to stop aging. After all, humans do not have to worry about molting as lobsters do, and human bodies naturally produce some telomerase that could be mimicked as a form of treatment. However, humans do not produce as much telomerase as telomerase has often been linked with higher rates of cancer. Never-ending telomeres are a double-edged sword; healthy cells can replicate ad infinitum, but it also means cancerous cells can do the same. Even without increased levels of the enzyme, extant cancers seen in animals, like humans, force the production of telomerase. This prevents these dangerous cells from dying out naturally and may make them resistant to some therapies which would put an end to the ordinary cell. By increasing the levels of telomerase in our bodies to try and combat aging, we might inadvertently make it easier for harmful cancers to develop. This effect has been demonstrated in mice who share many biological and physiological similarities with humans. Some researchers still hold out hope that curated parts of telomerase might be useful as an anti-aging remedy, but even if proven true, human aging is caused by a wide variety of other factors– many of which are yet to be understood.
*This article was originally published on the Stem Explorers (STEMx) website www.stemexplorers.net and submitted by the author to Broncology.
References
Osterloff, Emily. “Are Lobsters Immortal?” Natural History Museum, https://www.nhm.ac.uk/discover/are-lobsters-immortal.html. Accessed 7 Oct. 2023.
“Are Telomeres the Key to Aging and Cancer?” Learn Genetics, 2023, https://learn.genetics.utah.edu/content/basics/telomeres. Accessed 7 Oct. 2023.
Berthold, Emma. “The Animals That Can Live Forever.” Curious, 10 Sep. 2018, https://www.science.org.au/curious/earth-environment/animals-can-live-forever. Accessed 7 Oct. 2023.
De Magalhães, João Pedro, and Olivier Toussaint. “Telomeres and Telomerase: A Modern Fountain of Youth?” Rejuvenation Research, vol. 7, no. 2, July 2004, pp. 126–33. DOI.org (Crossref), https://doi.org/10.1089/1549168041553044. Accessed 7 Oct. 2023.
"DNA Replication (Updated)" YouTube, uploaded by Amoeba Sisters,28 June 2019, https://www.youtube.com/watch?v=Qqe4thU-os8. Accessed 7 Oct. 2023.
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