The actual title of Thomas’ article for August 6 is Useless Search for Evolution of the Human Brain, but the sentiment is clear. Now, I’m sure we can all agree that if you’re going to publish an article slighting an entire area of scientific study as “useless,” putting it out 30 minutes before a 1-tonne car rockets down onto the surface of another planet ranks high on the list of worst possible moments. But then again ignoring the rover completely may well be their best option there.
Thomas begins his poorly-timed article with:
Evolutionary scientists do not know how the human brain’s ability to process language supposedly evolved from a non-speaking ancestor. Recent technological advances have enabled scientists to explore this subject in new ways, and one researcher’s review reveals two flaws that underpin the whole research effort.
Gene discovery starts with an unusual, heritable phenotype, and then proceeds to determine the chromosomal locus of the mutation, and finally to identify mutated gene itself. Phenotype discovery starts with species differences in genes or gene expression, identified through gene discovery, comparative genomics, or other comparative molecular methods, and proceeds to identify the biochemical, cell-biological, and other phenotypic consequences of the genetic differences.
(The text in the figure itself is inexplicably in comic sans, so avert your eyes there.) We’re not talking about a ‘flaw’ here as such – the article does not contain that word at all – but a way to do things better/further areas of investigation.
Pruess gives a case study of the FOXP2 gene, which is a regulatory gene involved in human speech. The trouble is that it is mixed up in so many other things as well. Pruess discusses the wealth of investigation that has gone into figuring out the little we know about how the gene works and affects speech in humans, and how different techniques play into it. An important part of his message is that ‘it’s not that simple’ – but not that it’s impossible to understand.
Thomas seems to have entirely the wrong end of the stick:
Emery University’s Todd Preuss wrote “As a gene associated with a human-specific trait [speech], FOXP2 would at first glance seem to be a dream come true for evolutionary geneticists.” Could this be a language gene that explains how a human brain could have evolved from a chimp brain?
No. The high hope once held for FOXP2 as a key to explain the evolution of speech in the brain was dashed on the rocks of real research. Analyses of FOXP2 gene activity showed that it was not only used in brain tissues that facilitate speech, but also in various tissues throughout the body with a variety of uses. And a broad array of animals including all mammals, birds, fish, reptiles, and alligators share an almost identical gene—although none of those creatures talk like people.
This represents an overlooked flaw in the evolutionary research approach. Because FOXP2 turned out to be involved in many traits, its evolution by natural selection is highly improbable. Supposedly, nature “sees” and “selects” an individual with a certain trait. How, then, could a single natural environment select multiple traits at once?
The answer, as always, is the Thomas has no idea what he’s talking about. Natural selection is perfectly able to “select multiple traits at once,” and indeed has to all the time as a truly ceterus paribus situation is available approximately never. I’m having a hard time guessing how Thomas is visualising the process of natural selection. My best preforming idea is a reverse of the Mars Science Laboratory landing process, with a flying crane appearing overhead, picking up….something (I’m not sure – organism or ‘trait’?) and flying away to Evolutionary Labs (Inc.). It’s certainly nothing like the real world.
Regardless, Preuss continued to assert that natural selection, not God, designed organisms. He wrote of “whole-genome screens to identify genes that underwent human-specific sequence changes as a result of selection.” Scientists can indirectly detect if selection did not cause a gene.
I’ve split up this paragraph to highlight that last sentence. It makes no sense. Cause a gene what? To be created? Can’t be, as natural selection is analogous to the potter’s hands at his wheel – it does not make the clay, other processes are involved there. Anyway, finishing that paragraph:
But if they weren’t present in the past to observe any changes, how can any researcher know that human-specific genes were the result of selection or even that they were the result of any kind of changes? More likely, the DNA differences existed from the beginning.
“How do you know? Were you there?” There are ways to know, and Preuss covers them like so:
It has long been understood that the evolution of biological features that do not fossilize, including molecules, can be reconstructed by comparing appropriately chosen species. Human specializations are, by definition, features of the human species that evolved in our lineage after it separated from the lineage leading to chimpanzees and bonobos, our closest relatives. A claim about human specializations requires comparing the human species to its sister taxa (chimpanzee and bonobos), to demonstrate that there are differences between these species, and then comparing the human–chimpanzee–bonobo group vs. other apes and monkeys, to estimate whether the common ancestor of humans, chimpanzees, and bonobos resembled humans or chimpanzees and bonobos (Fig. 1). The more species that can be studied, the more reliable the evaluation of evolutionary change.
You need to compare them between species. As an example, he says:
The beginning of comparative molecular biology (at least as regards human evolution) is usually traced to Nuttall (1), who found that rabbit antisera raised to human blood reacted strongly with human, chimpanzee, and gorilla blood, but less strongly with orangutan or gibbon blood, indicating that the molecular differences between species are consistent with their evolutionary relationships as inferred from differences in anatomy (2).
A salient point in Pruess’ article is that it isn’t true that all the differences between humans and chimps are down to small genetic changes with large effects. This leads to two things relevant to previously discussed topics – first, on the subject of Tomkins’ claims that humans and chimps aren’t so close after all, Pruess said in the abstract:
It is now clear that the genetic differences between humans and chimpanzees are far more extensive than previously thought; their genomes are not 98% or 99% identical.
We are yet to hear however, how this is so damaging to evolution. In addition, the reduction is not as large as Tomkins claims:
One consequence of the numerous duplications, insertions, and deletions, is that the total DNA sequence similarity between humans and chimpanzees is not 98% to 99%, but instead closer to 95% to 96% (41, 48, 49), although the rearrangements are so extensive as to render one-dimensional comparisons overly simplistic.
The second is that we’ve heard a lot from the ICR about how there are apparently extensive differences in regulatory DNA (rather than genes) that cause the changes. That doesn’t seem to be the case.
Preuss wrote, “In neither case, however, do we have a direct connection between language and the specific FOXP2 substitutions [mutations] that took place in human evolution.” In other words, the gene does not directly connect to a trait that nature could select. So how could nature select the human-specific version of FOXP2 during “human evolution”?
The full quote in context is as follows, with what Thomas decided to quote bolded:
The fact that mutations of FOXP2 in humans result in speech impairments shows that it plays a role in speech development, but the nature of its role remains unclear. It might play a very specific role, for example, by orchestrating a whole set of genes that switch brain development from an ancestral program to a human program that causes cells and connections to differentiate into systems that sustain speech or language. It might even regulate the development of other parts of the anatomy, such as the lungs and larynx, involved in speech production. Alternatively, FOXP2 might have a permissive role, for example, by regulating some aspects of cell behavior required for the normal development of language systems, but also for the normal development of other structures and systems. Both options would be consistent with the action of a loss-of-function mutation in FOXP2, such as the R553H mutation in the KE family. In neither case, however, do we have a direct connection between language and the specific FOXP2 substitutions that took place in human evolution (T303N and N325S). There is not much question that these changes were the result of selection, and that they affect gene expression in the brain. However, given the widespread pattern of FOXP2 gene expression in the body, those substitutions are likely to affect gene expression in other organs, so it remains possible that the substitutions were driven by selection acting on non–speech-related parts of the brain or nonbrain tissues and organs. Humans are, after all, not just apes with unusually large, complex brains: other aspects of anatomy and physiology were extensively modified in human evolution as well. It could also be the case that FOXP2 has a speech- or language-specific function in the human brain, by virtue of the action of other transcription factors that bind to the same promoters in brain cells targeted by human FOXP2. However, then we would be talking about the interactions of genes involved in building a human organism, rather than a single gene, and it still would not be clear, without additional evidence, that the amino acid substitutions in FOXP2 were selected for their effects on developmental pathways specific to language.
It’s not direct – but that doesn’t mean its not there. It’s more complicated than that, but “There is not much question that these changes were the result of selection.”
The second flaw is the author’s reliance on a logical fallacy to support the concept of human evolution. It begs the question, which occurs “when a person merely assumes what he or she is attempting to prove.” Thus, the 2002 Nature report begged the question of evolution in their statement, “Our method suggests that the fixation occurred during the last 200,000 years of human history.” But the “method” the researchers used was force-fitting the FOXP2 sequence data into a diagram that assumes evolution.
As usual, that’s not begging the question. Evolution may indeed be a ‘premise’ here, but what is ‘proved’ is not that evolution occurred but when it happened. What’s more, as usual if this was indeed a legitimate complaint from Thomas it could be used on his own arguments elsewhere with devastating effectiveness – I’ll have to note it next time he tries to make a positive case for creationism.
Preuss and others did not mention—let alone test—the possibility that FOXP2 was purposely placed to serve multiple functions throughout many body tissues in many creatures. Creation science, however, does not suffer from either of the two flaws that characterized the FOXP2 investigation.
No, because a) they’re not actually flaws and b) creationism has plenty real ones of its own. And how would he have “tested” that, Brian?
This is a disjointed article that misses the point completely and would probably have been better left to Jeff Tomkins rather than B.T. – there would have been a small chance there that he might have made a bit more sense of the situation. Instead we have some non-problems raised (including the usual circular reasoning one which seems to be a fallback for him) and an entirely-overlooked ‘admission’ over the genetic similarities between humans and chimps. Wonderful – I wonder what else we have in store for this month?
The title of this post, for those of you who don’t know, is a parody of Andrew Schlafly’s catchphrase “Give it up, Liberals!” (Yes, he really does say that – see here for just one example.)