|Yipee! I've got 20 TP53 genes!|
Let's play a game and pretend there really is a magic invisible creator above the sky, like creationists and their pseudo-science version, Intelligent Design, want us to believe. What are we then to make of two research papers which could explain why elephants have such a low incidence of cancer? One team was led by Joshua Schiffman, a paediatric oncologist and scientist at the University of Utah, Salt Lake City, USA and the other by Vincent Lynch, an evolutionary geneticist at the University of Chicago, Illinois, USA.
Remember, although ID proponents are careful not to claim their supposed creator is the Christian god of the Bible or the Moslem god of the Qur'an, they are invariably religious fundamentalists who believe their holy book is the literal word of their god and so need to find plenty of gaps in which to fit their particular god. In both cases though, they believe their god is a benign, all-loving god who created everything for humans who it loves particularly as its special creation.
So, what do these pieces of research show?
Firstly, we need to consider something known as Peto's Paradox. In the 1970s, Richard Peto, a researcher at Oxford University, pointed out that, if cancers arise due to mistakes in DNA replication during cell division, we would expect cancers to be more common in animals with more cells, therefore, the larger an animal is the more cancers it should have on average. However, elephants, one of the largest mammals has on of the lowest incidence of cancers (about 3%) yet has vastly more cells than humans. Other researchers have found that there is no correlation between body size and the incidence of cancer.
Clearly then, there is not a simple relationship between the number of cell divisions and the probability of cancer developing, and yet the fundamental cause of cancer is undoubtedly faulty DNA replication, so something else must be happening.
What's happening is that a gene, TP53, has evolved which helps the body cope with damaged DNA but with varying success. It does it in two ways: firstly, it tries to repair the damage and, if that fails, it destroys the cell with the faulty DNA. Obviously, when a cancer still develops this mechanism has failed at both. In fact, what seems to happen is that failure of the repair stage isn't recognised as failure so the cell isn't destroyed.
What both these teams have shown is that, almost certainly through errors in DNA replication, elephants, including extinct species of mammoth, have multiple copies of this gene - some 20 in African and Asian elephants and over a dozen in extinct mammoths. This gives them much greater intolerance of damaged DNA and they seem to go straight for the cell-destruction stage without bothering to try to repair the damage first.
When you think about it, this is the fail-safe option which any benevolent intelligent designer, if had been so incompetent as to allow cancers to arise from imperfect replication of DNA in the first place, would have gone for. It's not as though there is a shortage of cells that every single one needs to be conserved especially when there is nothing to prevent another cell duplication if one goes wrong.
Additionally, the Chicago team have shown the even the elephants' closest relatives, manatees and hyraxes, have just one copy of the TP53 gene, so this multiple copying in elephants must have arisen after these groups diverged but before the living and extinct elephants diverged.
A major constraint on the evolution of large body sizes in animals is an increased risk of developing cancer. There is no correlation, however, between body size and cancer risk. This lack of correlation is often referred to as "Peto′s Paradox". Here we show that the elephant genome encodes 20 copies of the tumor suppressor gene TP53 and that the increase in TP53 copy number occurred coincident with the evolution of large body sizes in the elephant (Proboscidean) lineage. Furthermore we show that several of the TP53 retrogenes are transcribed and translated and contribute to an enhanced sensitivity of elephant cells to DNA damage and the induction of apoptosis via a hyperactive TP53 signaling pathway. These results suggest that an increase in the copy number of TP53 may have played a direct role in the evolution of very large body sizes and the resolution of Peto′s paradox in Proboscideans.*
TP53 copy number expansion correlates with the evolution of increased body size and an enhanced DNA damage response in elephants
Michael Sulak, Lindsey Fong, Katelyn Mika, Sravanthi Chigurupati, Lisa Yon, Nigel P. Mongan, Richard D. Emes, Vincent J. Lynch
bioRxiv doi: http://dx.doi.org/10.1101/028522
*Copyright: The copyright holder for this preprint is the author/funder. It is made available under a CC-BY-NC 4.0 International license.
So why are we playing this childish game of pretending the creationists' imaginary magic invisible sky friend is real?
Because it raises some important questions that creationists need to answer, apart from the obvious one about why an omnibenevolent designer would create cancers in the first place. Creationists normally handle that by either blaming the victims, by redefining 'good' to include inflicting suffering and death on people or with a shrug of the shoulders and asserting that they can't know their friend's mind even though they're forever telling us what it thinks.
The questions are:
- Why did it create cancer in elephants in the first place for which it then had to design a cure?
- Why did it design a not very effective cure for the cancer it had supposedly designed for most other animals?
- If it had intended the cure to work, assuming it couldn't reverse its cancer design for some reason, why didn't it make it more effective the way it has in elephants? It seems to have designed a cure for some species then forgotten all about it when designing the others?
- Has this omniscient designer designed cancer in elephants as a punishment for some 'sin' or other, like creationists claim it designed cancer in humans for, and then decided to forgive them?
- If so, why has it designed this cure for all species of elephant yet none of their closest relatives and made it look like the cure wasn't designed at all, but evolved in an earlier ancestor and was then inherited by descendant species, just as though there has been evolution by natural selection?
Of course, we're playing this childish game to show that the entire childish notion of species being designed, intelligently or otherwise, is simply unsustainable when you look at the details. There is absolutely no evidence of design in this system and, perhaps more importantly, no role for a designer in the explanation for it. Instead the entire thing can be explained quite simply by evolution by natural selection, without recourse to magic. The reason elephants don't get as many cancers as we would expect from the simple mathematics of probability and the number of cell divisions involved in growing an elephant, is due to a chance error in DNA replication back in their evolutionary history - ironically, a failure of the same faulty mechanism that gives rise to cancers in the first place.
The real questions for creationists to answer here then are:
- Why do you insist that no new information can arise by mutation when this gene multiplication has clearly resulted in new information?
- Why do you insist that mutations are invariably harmful when this one has been of such demonstrable benefit to elephants?
- Why do you reject the scientific theory of Evolution by Natural Selection when it gives a perfectly rational explanation to these sorts of phenomena, whereas the evidence-free notion you prefer raises more questions than it answers and leeds to absurdities such as these?
No, I don't really expect a coherent, rational explanation because one simply isn't possible within the creationist paradigm. Even thinking about this can cause serious cognitive dissonance.
- Abegglen LM, Caulin AF, Chan A, et al. Potential Mechanisms for Cancer Resistance in Elephants and Comparative Cellular Response to DNA Damage in Humans. JAMA. Published online October 08, 2015. doi:10.1001/jama.2015.13134.
- Sulak, M. et al. TP53 copy number expansion correlates with the evolution of increased body size and an enhanced DNA damage response in elephants
Reprinted in bioRxiv doi: http://dx.doi.org/10.1101/028522.
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