image source, Getty Images
Unlike humans, there are many animals that have tails.
- Author, Laurence D. Hurst
- Role, Conversation*
If one does a Google image search for the word “evolution,” one will see a large number of Ralph Zallinger’s famous illustration: the march of progress.
From left to right, we see a chimpanzee walking on its knuckles as it gradually develops into an upright human-like gait.
Implicit in these images – and in the photograph’s title – are the prejudices of the common view of evolution: that we are a species at the top of the evolutionary chain, the perfect product of a process.
We imagine that we are the fittest survivors, the best that we can be. But seen this way, there is a paradox. If we are so amazing, how is it possible that so many of us suffer from genetic or developmental diseases?
A new study, published in the journal Natureoffers an explanation for our error-prone early evolution by analyzing the genetic changes that allowed our ancestors to lose their tails.
image source, Getty Images
Rudolph Zallinger’s illustration, The March of Progress, spawned a million imitations.
Current estimates suggest that approximately half of fertilized eggs never become a recognized pregnancy, and that for every child born, about two never reach term.
Such an early death is unheard of in fish and amphibians. Of those of us lucky enough to be born, less than 10% will suffer from one of the many thousands of “rare” genetic diseases such as hemophilia. Less rare diseases like sickle cell disease and cystic fibrosis affect even more of us.
Would this happen in a species with such evolutionary success? Where is the progress?
There are several possible solutions to this problem. One is that we have an unusually high mutation rate compared to other species, so there’s a pretty good chance that there’s something in your DNA. a change neither your mother nor your father inherited.
You were probably born with ten to a hundred new changes in your DNA. For most other species, this number is less than one, and often much less.
The genetics of tails
One of the most obvious differences between us and many primate relatives We just don’t have a queue.
The loss of the tail occurred about 25 million years ago (for comparison, our common ancestor with chimpanzees was about 6 million years ago). We still retain the coccyx as an evolutionary remnant of this tail-bearing ancestor.
The loss of this limb occurred in our ape ancestors at the same time as the development of a more upright back and, subsequently, a tendency to use only two of the other four limbs to support the body.
image source, Getty Images
In fish and amphibians, mortality during fertilization is much lower than in humans.
While we can speculate as to why these evolutionary changes may be associated, this does not address the issue of how (rather than why) tail loss evolved: what were the underlying genetic changes?
A recent study addresses this very question and has identified an interesting genetic mechanism: fact Many genes combine to allow tail development in mammals.
The team discovered that tailless primates have an additional “jump gene” — DNA sequences that can be transferred to new regions of the genome — in one of these tail-determining genes, TBXT.
Much of our DNA is left over from those jump genes, which are proteins that specify their frequency (the classic function of genes), so gaining a jump gene is nothing special.
The cost of evolution
What was unusual was the effect of this new addition. The team also found that the same primates also had an older but similar very short-distance jumping gene in their DNA, inserted into the TBXT gene.
The proximity of these two genes altered messenger RNA processing resulting from TBXT (molecules made from DNA that contain instructions for making proteins).
Two jump genes can stick together in the RNA, causing the block of RNA between them to be excluded from the protein-coding RNA, resulting in a shorter protein.
To see the effect of this unusual deletion, the team genetically mimicked this situation in mice by creating a version of the mouse TBXT gene that also lacked the deleted part. And indeed, The larger the form of RNA with the gene section knocked out, the more likely the mouse was born without a tail.
This offers a strong theory of the mutational change underlying the evolution of taillessness.
But the team noticed something else strange. If a mouse is created with only a form of the TBXT gene with a portion deleted, it can develop a condition very similar to human spina bifida (where the spine and spinal cord do not develop properly in the womb, causing a spina bifida).
image source, Getty Images
X-ray of pelvis and lumbosacral spine with spina bifida.
Mutations in human TBXT have previously been associated with this disease. And it should be noted that other mice also had various spine and spinal cord defects.
The team suggests that, like the coccyx, it is an evolutionary continuation of the lack of a tail that we all have, spina bifida may be a rare sequel to the gene change that underlies our lack of a tail.
Not having a tail, they suggest, was a huge advantage, so the increased incidence of spina bifida was still worth it. This may be the case with many genetic and developmental diseases: they are the occasional byproduct of some mutation that helped us along.
For example, recent work finds that genetic variants that help us fight pneumonia They also predispose us to Crohn’s disease.
This shows how deceptive the march of progress can be and that evolution can only deal with the variations present at any given moment.
As this latest study shows, many changes come at a cost, which can be seen less as a march and more like a drunken stagger.
* Laurence D. Hurst is Professor of Evolutionary Genetics at the Milner Center for Evolution, University of Bath, UK.
*This article was published on The Conversation and reproduced here under a Creative Commons license. click here to read the original version and view links to cited studies.
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