Elephant's Revived Zombie Gene Fends Off Cancer
One would suspect that elephants, being as large as they are, would be especially susceptible to cancer. The sheer number of cells that make up an elephant is substantially more than many animals, leaving a greater possibility for cell division to go wrong and cancerous mutants to arise. Elephants, however, surprisingly present the same risks as any other animal, including humans. It was recently found that this may be due to particular genes that protect them against cancerous cells, including not only a more prominent form of the well-known tumor-suppressing p53 gene but also new protein known as LIF6.
The pathway works with a response from the 20 copies of p53 genes present in elephants (humans only have one copy!). When DNA damage is detected, rather than attempting to repair it, they instead turn on LIF6 which creates proteins that move to the mitochondria and essentially pokes holes in it, thus leading to the cell’s death. This aggressive attack on damaged cells is unique to elephants as they are the only holders of the active LIF6 gene.
A New York Times article discussing this particular gene refers to it as a ‘Zombie Gene’, and for good reason. This gene has seemingly come back to life in elephants after remaining dormant in many mammalian species. This means that this gene, although it exists in many mammals including humans, has been nonfunctional throughout evolution as it cannot create the LIF6 protein. Elephants, however, have at some point in their evolution resurrected the LIF6 gene and it is now able to be turned on by p53 and produce this new, remarkable response.
It is estimated that this LIF6 gene arose at around the same time extra p53 copies arose in elephants’ very early ancestors nearly 80 million years ago. It is also thought that other mechanisms against cancer have likely evolved in elephants and that such powerful defense mechanisms against cancer that have arisen have allowed for elephants to evolve to such great sizes. Further research on these magnificent animals may help us to better understand the cellular processes behind cancer, as well as potentially aid in the development of new drugs and treatments for the disease.
Posted by "Alexandra Rios" (3)
That's pretty cool! You have to wonder, though... This LIF6 gene seems like a pretty good thing... For elephants it seems to work out great. Why has it functionally disappeared from most genomes? There must be some bad effect that we don't know about... It seems too good to be true.
ReplyDeleteChandler Kupris
Yeah, you may be right! I wonder be curious to know more about whether this gene could actually work in humans/other mammals and provide the same benefits we see with elephants. I would be interested in seeing if they are able to answer this question in the future!
DeletePosted by Alexandra Rios
I always find it interesting when we look to other mammals for "inspiration" of sorts. This gene seems like it could lead to some serious developments and knowledge in the cancer field, but if it is so advantageous, why would the gene fall dormant in so many other species? This also leads me to wonder if there are other cancer preventing genes unique to other animals that we just have not been able to or thought to identify yet. There is so much out there to explore and learn and looking at other animals seems like a logical place to find intriguing new information!
ReplyDeletePosted by Jamie Downer
I agree. Other animals are a great source of information. It seems that they also believe elephants may have other mechanisms to protect themselves against cancer so that would be great to look more into as well. I definitely think the research that can be done on all kinds of animals would be worth trying!
DeletePosted by Alexandra Rios
when the cell has a programmed cell death it is called apoptosis. i hear lot of different mechanisms and pathways for apoptosis, but this the first time i read about the mechanism of LIF6. In poking holes in the mitochondria disrupt its function which can be defined as cell suffocation, because the cellular respiration is affected and as result the cell dies. This is a terrible way to kill a cell but if the cell is a cancer cell, which is important for elephant survival, it is beneficial.
ReplyDeletePosted by Jad Imad
Its mechanism is pretty drastic. I hadn't heard of cell suffocation before so this was pretty interesting to find out. Immediately killing the cell seems like the most logical solution though and its great that this has worked to protect them.
DeletePosted by Alexandra Rios
I have studied p53 extensively, but never before heard of LIF6! Do we know what has caused these genes to become active again? If many other mammals carry this same gene, I wonder what sort of selective pressure would have caused this gene to become active again in elephants specifically.
ReplyDeletePosted by: Hayley Fecko
I am curious as to the ways in which LIF6 is regulated and whether or not this has an effect on how it is activated and/or deactivated in mammals? Could there be some sort of regulatory mechanism that is present in elephants that became active again that is not present in humans?
ReplyDeletePosted by Lauren Hiller
It is a really interesting post. I think this more prominent form of p53 tumor-suppressor and the LIF6 protein were two essential adaptations that helped elephant defense cancer with giant body size. Without these genes, elephants may not be so large. I am also surprised that the LIF6 genes was actually non-functional in other mammals, but elephants had this genes reactive.
ReplyDeleteReplied by Muchen Liu
You mentioned in your opening paragraph that because of the elephant's size, it would be thought that they would be more susceptible to and have a higher frequency of cancer. It seems as though it could be plausible since a larger animal has to undergo cell division more often. Although that kind of logic is intuitive, is it true? If it is true, that is possibly why elephants have developed the LIF6 protein and the multiple copies of p53 in their evolution.
ReplyDeletePosted by Jamie Courtney