On the genetic foundation of language

Niccolo Caldararo wrote:

Language does not rely on the present physiology of speech as many of those involved in animal research have shown, as American Sign Language proves, as the "click languages" demonstrate. The mistake the authors of this article make, and which is made over and over again in the realm of what is called molecular anthropology is the belief that single gene changes are additive, that somehow a few gene changes and you can go from a chimp to a human.

---------------

Bear in mind that I'm not arguing with your last statement here, but thought you might find this an interesting sidelight.

From Klein & Takahata, _Where Do We Come From? The Molecular Evidence for Human Descent_, Springer-Verlag 2002, p203-4.

“Once the molecular differences between humans and chimpanzees are known and those responsible for the distinctiveness in appearance are identified, what will they be like? In the absence of any hints from comparisons between other species (in no pair of species have the differences in appearance been explained at the molecular level) one can only guess. From the study of mutations that alter the adult phenotype of humans and other mammals, as well as from the analysis of mutations that alter the development of model organisms, it appears that almost any morphological character is the result of a complex molecular pathway which involves large cohorts of genes. Mutations in many of these genes may lead to an alteration or disappearance of the character even though all the other elements of the pathway remain in place over long periods of time, presumably because they also participate in pathways leading to other characters. In the same way as a character can be lost as a result of a single mutation, it can also be regained if the function of the mutated gene is restored by another mutation. The return-to-function mutation can either take the form of a reversal of the original change or that of a different mutation that compensates for the effect of the first one.

The reappearance of a character believed to have been present in a remote ancestor is known as atavism (from Latin atavus, ancestor). The resurrection of the character indicates that the complex pathway leading up to it is still intact and that even the gene responsible for the loss of the character is still present in a form that can be reactivated. Extrapolating from these observations it can be speculated that the assembly of the pathway leading to a particular character began long before the actual appearance of this character. The various elements of the pathway in question may gradually have become available from other pathways, but only when the final element appeared did the new pathway become functional. In this manner, a complex character may not just be lost, it may also appear to have been created in a single step, in an extreme case by a single mutation. Small changes at the molecular level would then appear to have a great impact on the appearance of the organism at the morphological level.

To put some flesh on the bones, consider, as an example, human nakedness. One of the characteristic features accompanying the emergence of mammals from theriodont reptiles was the appearance of hair on the outer body surface. A hair is in essence a long column of keratinized cells growing out from an onion-like nest in a deep pit in the skin, the hair follicle. The stimulus to form a hair follicle ensues from the interaction of two principal skin layers, the outer epidermis, which is of ectodermal origin, and the inner dermis, which is derived from the mesoderm. The long and complex pathway, from the initial interaction of the two tissues to the appearance of a mature hair, involves many genes. They are genes that determine the distribution of the sites in the skin at which the interactions leading to hair follicle formation occurs; genes that code for proteins involved in these interactions; genes that control the cell divisions by which the hair column grows and that determine the column’s shape, length, and color; genes responsible for keratinization of the column; and genes that coordinate the entire process.

The reptilian ancestors of mammals lacked hair but possessed scales which, like hair, are produced by the interaction between the epidermal and dermal skin layers and which, again like hair, are formed by a complex developmental pathway. It is highly unlikely that the hair-growth pathway was assembled from scratch through the evolution of brand new elements. It is far more probable that it arose by modification of the scale-growth pathway supplemented by the recruitment of elements from other existing pathways.

There can be little doubt that the ancestors of humankind had bodies which were covered by a coat of hair similar to that found in other primates. The strongest evidence of this is the observation that rare atavistic mutations lead to the recurrence of hair growth in humans to produce a coat of hair resembling that of certain other primates. Since the Middle Ages, some 50 cases of a condition clinically classified as generalized congenital hypertrichosis have been recorded (Greek hyper, above, over; thrix, hair; here “congenital” means “hereditary”). Some of the unfortunate sufferers of this disorder were cruelly paraded in circuses or at exhibitions as “human werewolves”, “hair men”, “dog men”, or “ape men” because most of the surface area of their bodies was covered by dense hair as observed in our ape ancestors. In one of the best studied cases involving 19 individuals of a Mexican family, the origin of the condition could be traced back to a gene on the X chromosome. Presumably a mutation in this gene restored its function and thus initiated the expression of the pathway leading to full hair cover. This pathway must therefore still be intact in every one of us and it takes only a small step to its manifestation.

The difference between possessing a coat of hair or appearing naked is actually far less dramatic than most people think. We are not really “hairless” on most parts of our bodies; in fact, we have almost the same density and distribution of hair follicles in our skin as chimpanzees or gorillas. Most of our body hair is generally much shorter and finer, however, so that it is almost invisible. Regardless of the mechanism responsible for the transformation from clearly visible to almost invisible hair, the cases of hypertrichosis demonstrate that this mechanism can be flipped on or off rather easily at the molecular level. This may also hold true for many other molecular mechanisms responsible for the sapientine characters of our species. The impression of a gap between the small differences at the molecular level to the seemingly large differences at the phenotypic level may arise because the intervening steps between the genotype and the phenotype, between the DNA and the appearance of an organism, remain unidentified. It will be thrilling to find out what these small difference really are, to identify the genes in which they reside, and to see how they are translated into the ability to speak, to walk on two feet, or to write this sentence.”

JG