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by Lloyd Pye


A short segment of DNA recovered from the Starchild Skull is a close match to the human FOXP2 gene, a gene essential for proper organ development, speech, and a host of other important functions. The result is preliminary and unverified (this DNA segment has only been recovered once when it needs to be recovered dozens of times for positive proof), but in a section of the gene that is virtually 100% identical in all humans, the Starchild Skull DNA had 56 differences from the human FOXP2 gene. No human has a gene with so many differences from normal, and realistically it would not be possible for a human to survive even 4 or 5 differences, let alone 56. If this result is confirmed it will help to prove the Starchild Skull is definitely not human.



In 2012 a small section of DNA from a sample of the Starchild Skull was linked to a highly functional "master gene," one of the most vitally important genes in the body of any species on Earth. Virtually any complex species has a variation of this gene, and it is without question one of the most highly conserved genes in the human body (it is virtually identical in all humans). It is the FOXP2 gene. That odd name comes from its technical title: Forkhead Box P2, or FOXP2.


In any creature, the overwhelming importance of their FOXP2 gene is that it controls a "downstream" cascade of genetic processes in hundreds of other genes, all coordinating the formation of various parts of a body as it gestates and grows to maturity. In mammals and other "higher" species, any single flaw in FOXP2, any isolated mutation or variation, can cause a severe negative impact in some of the most important aspects of development: the function of the brain, the sound or speech mechanisms, the lungs, heart, guts, and nerves, among others. Because it is so utterly vital, it is even more highly conserved than mtDNA.


Recall that in the 16,569 base pairs found in the mtDNA genome of normal humans, as many as 120 variations can be found in the first of us, southern Africans. That percentage of difference is quite small, only 0.7%. Compare that with the FOXP2 gene, which in normal humans is 2,594 base pairs long, and contains no variations. 0%! None! Nada! Every normal human has the exact same array of FOXP2 base pairs as every other normal human.


This is not to say mutations never occur in FOXP2. They can and do, and a number of them have been found. However, every mutation is debilitating in some way, and because FOXP2 is vitally important to so many bodily functions, most mutations in it will cause termination of life. When termination does not occur, the mutation's impact on its host is usually severe.


In one well-studied mutation in the section of the gene that influences speech development mechanisms in humans, those who inherit it will never be able to speak. This has led some to suggest FOXP2 is a language gene, or a speech gene, but that is not the case. Speech is much too complex an arrangement of working parts to be so simply controlled, although a properly functioning FOXP2 gene is an essential part of the speech-development equation.


The key point to understand is that while a tiny amount of survivable mutations are possible in FOXP2, every one that occurs presents debilitating or life-threatening consequences, so to this point in time none have been passed on to the general population of humans. Therefore, in the vast, vast majority of humans, the FOXP2 master gene is absolutely identical.

With that said, let's examine the fragment of Starchild Skull FOXP2 sequenced by our geneticist. Of the entire 2,594 base pairs of the normal FOXP2 gene, our fragment is 211 base pairs that come from a segment near the center of the gene. If the same 211 base pair section were isolated from any normal human, every base pair would be exactly the same as what is found in any other human. There would be no difference in any of them.


Below: Section of Starchild suspected FOXP2 DNA (SCFOXP2?), compared to the same section of other species


Okay, ready....brace yourselves. The Starchild's 211 base pair FOXP2 fragment has a grand total of 56 variations! Now, while extrapolating this 211 base pair fragment is a bit more of a stretch than extrapolating the four combined fragments of mtDNA we discussed earlier, doing so does provide something to think about. Divide 2,954 by 211, and you get 12.3. Multiply 12.3 by 56, and the range of total variations in the Starchild's FOXP2 base pairs would be 600 to 700! So let's be crazy conservative and say it's only 200 or 300. It is still astounding in a super highly conserved gene that in normal humans has no variations at all!

If we compare the same section from a rhesus monkey's FOXP2, only 2 of its 211 base pairs would vary from any human. If it were a mouse, it would be 20. If a dog, 27. An elephant, 21. An opossum, 21. A Xenopus (a kind of frog), 26. So dogs and frogs are the most different, at 27 and 26 base pairs respectively.


To put this in perspective, let's imagine that when alive, the Starchild was indeed some unknown humanoid. No matter how different from humans it might have been, to be in the humanoid family its FOXP2 gene would have to be in the range of 1 or 2 or at most 3 base pair variations from a normal human. To go past 5 or 10 would put it into another class of species. 20 to 25 would put it in the range of mice and elephants, and dogs and frogs. To have 56 is to put it in another realm, another dimension entirely. It is utterly unique.

To verify this radical statement, below is the actual comparison of the Starchild's FOXP2 fragment with the same gene segments of some of the species listed above. In each case, imagine it as a string of 211 base pair nucleotides, although to fit into this format it must be broken into two segments, top and bottom. Notice the steady blue of the human nucleotides that make up its base pairs, and the stark red of each variation in the other species.


Notice the SCFOXP2 line directly above, beginning with "Gln." It lists the amino acids determined by three-letter codons. Codons establish rules by which information carried by genes is translated into proteins, which are molecules that perform various functions in cells and eventually in bodies. These groupings, known as triplets, are formed from the single-letter nucleotides—C, A, G, T—and they represent a blueprint for building the proteins that are encoded by each gene, using the standard set of 20 amino acids that our bodies utilize.


The fragment shown above encodes a peptide (a stretch of amino acids) that is very unusual in the human FOXP2 gene. It contains a long stretch of 40 triplets, each coding for the same one of the 20 amino acids—glutamine (Gln), encoded by either a CAA or CAG triplet. After the stretch of 40 Gln in a row, there is a shorter stretch with six other triplets and one more Gln, then another stretch of 11 Gln in a row. In the Starchild FOXP2 fragment, there is also the 40 Gln tract, plus the 11, but it also contains several more glutamines.

In the 211 base pair fragment from the FOXP2 gene in normal humans, no variations occur among the amino acid sequence in the FOXP2 protein, and the coding pattern for Gln (using either CAA or CAG) is exactly the same not only in humans, but essentially in all primates. (Compare only 2 amino acid variations in a rhesus monkey, which is not even a great ape.)


In the Starchild Skull, we find 16 amino acid variations in this fragment, which despite all those differences unmistakably resembles the human FOXP2. Yet it demonstrates a coding pattern that is wildly different from all species shown above. This is an astounding contrast!

Notice, too, the Starchild's 40 Gln stretch continues for 3 more, making it a 43 Gln stretch, where it reaches what is known as a "stop" codon, TAG, signified by the blue all-cap STP near the middle of the bottom line. The presence of this "stop" codon inside the protein is quite strange, since it will result in production of an abnormally shortened FOXP2 protein devoid of the downstream regions that are critical for important functions of this protein.


It is always possible that some kind of sequencing error has been made, so it needs to be repeated to confirm this initial analysis. In any case, after the mysterious "stop" codon, a new Gln stretch begins and continues to only three amino acids from the fragment's end. This, too, is wildly different from the human sequence, but as with the other anomalies, further research is needed to determine what altered functions these differences cause.


Another comparison to make is to remove the Gln stretches from different species and examine what is left. For example, if we analyze the entire FOXP2 gene in humans and chimps, our closest genetic relative, with the Gln stretches removed from consideration, then only 2 amino acids (depicted by the three-letter codons) are different. The same 2 are found in gorillas and other higher primates. In mice, the difference is 3 amino acids.


If we remove the Gln stretches from the Starchild's fragment of FOXP2, only 7 amino acids remain to be compared to the corresponding amino acids of the human FOXP2. These are the first four, at the beginning of the fragment, and the last three, the end of the fragment, and all 7 amino acids are different! Whatever we might say about this comparison, it is certainly not between two humans, or anything near two humans.


In addition to having a "stop" codon in its last quarter, the Starchild fragment is also missing the large intron (marked with a vertical green arrow) that normally intervenes in the human gene and in the gene of other species. This suggests that the Starchild fragment could be a pseudogene, dysfunctional ancestors of normal genes that have lost the ability to encode proteins, or are otherwise no longer capable of being expressed in a cell. This means they are nonfunctional, and are therefore another form of junk DNA.

Suggesting the Starchild's FOXP2 fragment might be a pseudogene immediately collides with the fact that there is no currently known human FOXP2 pseudogene. Because it is a master gene, it must always function properly, and if it doesn't function properly in even a small way, very negative things happen to the individual carrying the variation. Thus, since a human FOXP2 pseudogene is not known to exist, if it turned out that the Starchild Skull carried one, that would clearly establish it as not human.


What's the bottom line? That can only be determined when the entire Starchild genome is recovered and compared—nucleotide by nucleotide, base pair by base pair, codon by codon, amino acid by amino acid—with humans, Neanderthals, Denisovans, chimps, and gorillas. Whatever it is, most of the preliminary evidence indicates it is quite distinct from humans.


Most important, perhaps, to keep in mind is that our FOXP2 results are preliminary, as are the results from the earlier nuclear DNA fragments, and the mitochondrial DNA fragments. All three preliminary results are highly indicative of what the final result will be, but they cannot be considered absolute proof. They can, however, be considered proof that absolute proof will come when the Starchild's entire genome can finally be recovered.

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