Why don’t humans have tails? Scientists find answers in an unlikely place
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About 25 million years ago, a change happened to put humans on an evolutionary path different from monkeys. The group of animals called Old World monkeys had tails, but a new group did not. That group later became gorillas, chimpanzees, baboons, orangutans, and humans. None of them have tails. But we have tailbones, so why not tails? How and why did this happen?
Monkeys can be divided into two groups depending on where (and when) they originated. Old World monkeys came from Europe, Africa, and Asia, which were the older parts of the world that were known to the Europeans at the time. After they set out to explore, they discovered places like North and South America, known as the New World. So, New World monkeys came from there. What is confusing is that on the evolutionary calendar, New World monkeys are older; they originated about 40 million years ago as a splitting off from other primates of the time. Old World monkeys spun off the New World monkeys about 25 million years ago. The majority of both types of monkeys had tails, and they are called the non-hominoids.
Hominoids grew out of the Old World monkeys. They include what are now called the Great Apes (humans, chimpanzees, gorillas, and orangutans) and the Lesser Apes (gibbons). The hominoids are different from the non-hominoids in having the following characteristics:
- generally larger brains relative to body size compared to other primates
- more flexible shoulder joints
- increased reliance on vision than smell
- longer gestation and maturation periods
- no tails
Tails themselves can be divided into two categories for primates: prehensile and non-prehensile. Prehensile tails can be used for grasping objects (fruits, branches), while non-prehensile tails can't. Generally, Old World monkey tails are non-prehensile and are used mostly for balance or social signalling (baboons, macaques). Most New World monkey tails are like that, too (marmosets, squirrel monkeys), but some are prehensile (spider monkeys, howler monkeys) and act like an extra hand.
What about the Great and Lesser Apes?
They have tailbones, called a coccyx, which is comprised of 3-5 fused vertebrae at the end of the spine. They are about 6-9 cm (2.5 to 3.5 inches) long. There doesn't appear to be any examples of intermediate forms of apes with shorter and shorter tails, so the number of vertebrae must have changed suddenly to produce the tailless apes.
Scientists at the Broad Institute (a collaboration between MIT and Harvard) think they have discovered the genetic cause of tail loss in Great and Lesser Apes. A team led by researcher Bo Xia examined DNA of 15 species of monkeys with tails and 6 species of tailless apes (including humans). They were looking for a mutation in the human and ape DNA compared to monkeys.
That sounds like a big task because of so much information in DNA. However, the following primates' DNA has been completely sequenced (read to make a list of all the nucleic acids):
- humans (2003)
- chimpanzees (2005)
- rhesus macaques (2007)
- orangutans (2011)
- gorillas & bonobos (2012)
- gibbons & marmosets (2014)
Scientists already know what 60% of human DNA functions are, and that includes mostly useless parasitic genes from viruses. But there is still about 40% that has an unknown function, so until it is learned, that is called "junk DNA". Xia's team didn't find any answers in the DNA with known functions, but the junk DNA provided the clue.
In the code of a gene called TBXT, which is associated with tail length, there was a flaw. A piece of junk. There are short fragments of DNA called Alu elements, that copy themselves like a virus, then jump around and move the copy to a new position in the DNA. Its only function is to do this. Humans have a million Alu elements scattered throughout their DNA, making up half of its content! That probably explains why humans are born with 10-100 mutations (mostly harmless), compared to the <1 mutations in other species.
These "jumping genes" can be mildly or severely troublesome. They can cause breaks in DNA, carry pieces of other DNA with them, disrupt the normal function of a gene if they land in the middle, and increase the mutation rate. They can be as small as a few hundred base pairs long (the nucleic acids on both sides of the DNA double helix) or a few thousand. Human DNA has about 3 billion base pairs.
A specific junk Alu element called AluY was found only in hominoids inside the TBXT gene. Finding this was remarkable enough. But TBXT already had a jumping gene like monkeys with tails do, but it did nothing. Was this extra one AluY somehow the cause of losing a tail? Xia and his team spent 4 years looking at the effects of both jumping genes in mice. They found that when they put the two jumping genes close together, they stick to each other and cause problems when the tail is made. A hole is formed in the TBXT tail protein, and the mouse's tail becomes shorter. The more of the damaged protein that is made causes the tail to become shorter by reducing the number of vertebrae in it.
None of this explains why the natural mutation in the TBXT gene was actually successful. Apes including humans began walking upright without the need for a tail to balance on, to signal each other, or to grab onto branches. But, the two oldest hominoid fossils found in Kenya dating to 21 million years ago and 18 million years ago (Proconsul and Afropithecus) show that even by then there were no tails. They lived in trees and walked horizontally. So, just leaving trees did not prompt the jumping gene mutation. And since there are no intermediate hominide fossils showing a shorter and shorter tail, this happened suddenly and persisted for some unknown reason.
Human embryos 4-6 weeks old have tails about 10-13 vertebrae long, but they almost always disappear by the eighth week. In extremely rare cases, children are born with a tail-like appendage, when the embryonic one is not naturally absorbed during fetal growth. Some have bones, others don't. They are all easily removed.
Whether the loss of a tail meant some evolutionary advantage is still uncertain. But the mutation from the pair of jumping genes in the TBXT DNA has a potential disadvantage that medical researchers might be able to investigate further. Some of the tailless mice in the study developed spinal column defects resembling spina bifida in humans. Spina bifida is a condition that occurs when the backbone doesn't completely form in specific areas, so the spinal column is not protected and will deform. The research on the TBXT gene mutation suggests spina bifida might come from the same mutation that eliminated tails. Medical science now has a stronger handle on its cause and might be closer to a solution.
Proconsul coccyx and explanation of why it appears tailless (4:00)
