The advent of complete genomic analysis has given rise to some fundamental questions in genetics. Among them are: (1) the human genome has only about 20,000 genes. If this is the complete blueprint, how can a complex body arise from such meager information? (2) the human and chimpanzee genome differ by only about 1%. How can such a wide species gap in the phenome arise from a genomic difference of only 200 genes?
The latter is the principal question in Steven Mithen’s review of Thomas Suddenhdorf’s book “The Gap”, and also plays a role in Svante Paabo’s book “Neanderthal Man” in the same review (NY Rev. Books 4.3.14). Mithen says “ultimately the gap must derive from differences in the genomes.” this seems obvious but avoids the two questions above.
I suggest that we are more than the sum of our genes acting individually, i.e. that in addition to traits coded in the DNA, extra-genetic traits not coded there are also essential, and more numerous. “Extra-genetic” includes epigenetic, i.e. chemical modifications in genes such as methylation that preserve the gene sequence but modify their effects, and also emergent properties, i.e. phenotypic modifications that emerge from combinations of genes rather than just the sum of traits from individual genes. An example is the observation that implanting a mouse eye gene into flies produces flies with extra eyes in the wrong places, but they are fly eyes, not mouse eyes. Clearly, while the mouse eye gene is active in flies, it doesn’t act alone, but rather in concert with numerous other unmodified genes which together create an unprecedented new morphology, ectopic eyes There are innumerable possible combinations of 200 new genes with all the other genes shared by humans and chimps, and this could easily account for the huge interspecies gap.
There is another, totally different possible contributor to this gap: the mother. Do signals from her body, independent of the fetus’s genome, influence morphology during gestation? If they do, then the species gap resides not only in differences in our genes, but also in what species the mother is. To suggest that the mother influences our morphology is not absurd, for we know that tiny amounts of substances, e.g. thalidomide, transmitted through the placenta profoundly influence the phenotype but not the genotype of the baby. Since the mother normally transmits thousands of substances to the fetus, perhaps many of them influence its phenotype independently of its DNA.
A test of this question would require implantation of a trophoblast into a female not the mother who differs from her in some way, and then seeing whether any of the foster mother’s traits appear in the newborn.