As humans, we often like to think of ourselves as being at the top of the totem pole of the animal kingdom. The large number of species we have domesticated is prime evidence for this. However, when we look at the cellular changes associated with domestication, it turns out we may have more in common with these tamed animals than we imagine.

Domestication can be thought of as permanent changes to the genetics of an organism that lead to an innate tendency to remain calm in the presence of humans when compared to its wild counterparts. Going further, domestication syndrome refers to the resultant observable changes caused by these genetic differences. Examples of these include smaller brains, floppy ears, smaller teeth, patches of depigmentation, juvenile facial appearance, and docility. Perhaps the most obvious example comes through canine species – easily seen when comparing the somewhat vicious appearance of wolves to the more endearing dogs we keep as pets.

Darwin first popularised domestication syndrome, but his attempts to explain how it came about largely focussed on how the environment of domesticated animals induces the traits observed. The fact that, when returned to the wild, domesticated animals do not regain ‘wild type’ characteristics and are therefore unable to survive refutes this theory. Later studies correlated the more docile behaviour of domesticated animals with reduced functioning and size of various glands in the body. However, until recently, there was no unifying mechanism to explain the hodgepodge of effects that result from domestication.

A potential explanation comes from examining the development of vertebrate embryos. Neural crest cells (NCCs) are stem cells that migrate to different areas within the embryo to form a variety of cell types. Cells derived from NCCs include those that go on to form the adrenal glands, skull, teeth, and the peripheral nervous system as well as those that go on to influence facial structure and skin pigmentation. Considering these cell types and their functions, we can see that they correlate notably with areas of the body physically affected by domestication syndrome.

NCCs could even provide a mechanism to understand the behavioural changes underlying domestication. An analysis of dog and wolf genomes found hundreds of genes that could potentially be involved in domestication. 27 of those had evidenced or hypothesised roles in NCC or central nervous system pathways. The mechanism behind this likely stems from the medulla of the adrenal glands, which is NCC derived. This endocrine organ secretes adrenaline – the hormone critical to the fight or flight response. Domesticated animals have been found to have smaller adrenal glands and lower levels of cortisol - the ‘stress’ hormone released by adrenal glands. Possible reduced adrenaline and cortisol levels give a viable explanation for the connection between neural crest cells and tameness.

“Coordinated punishment could have limited the reproductive success of highly aggressive individuals... [but] our ability to carry out proactive violence has arguably improved”

Interestingly, mutations affecting neural crest cells are also found in the human genome, despite being absent in our predecessors (the Neanderthals and the Denisovans). BAZ1B is one such gene, playing a major role in facial development. Mutations in the regulatory region of this gene mean that it is present in smaller amounts in human embryos, ultimately decreasing the efficiency of NCC migration to the facial region. This contributes to the relatively juvenile appearance of modern humans – we have smaller skulls and less pronounced brow-ridges.

Evidently, domestication is a process that evolves many genes and one mutation is not enough to be conclusive. However, BAZ1B has also been implicated in the more juvenile appearance of dogs compared to wolves, seeming to be a master regulator of facial development. In addition, BAZ1B is one of over 25 genes in a region of the genome which, when deleted in humans, results in Williams-Beuren syndrome. Symptoms include extreme friendliness and facial dysmorphism – hallmark features of domesticated animals. By contrast, duplication of this region leads to increased physical aggression and facial dysmorphism, arguably wilder traits.

Ultimately, what this suggests is that just like dogs, humans underwent a process that selected for individuals that were less aggressive. As humans formed more complex societies, it is possible that mates that displayed less reactive aggression (violence that was responsive and not targeted) were favoured. In bonobo (a type of primate) societies, groups of females are able to come together to suppress violent males. Perhaps in humans, similar coordinated punishment could have limited the reproductive success of highly aggressive individuals. Of course, our ability to carry out proactive violence (planned and targeted) has arguably improved, hence why humans have been dubbed the deadliest species on earth.

Self-domestication is not necessarily unique to primates – it is theorised that wolves that were less aggressive outcompeted the more aggressive ones by being able to get closer to humans and take advantage of the food, shelter and resources provided. Although humans certainly intervened at some stage, as evidenced by the large number of dog breeds today, it may be that dogs played a more active role than is commonly thought in becoming man’s best friend.

So, NCCs show how in selecting for tameness a whole host of other features can arise. Although further research is needed, there are certainly genetic similarities in genes associated with NCCs in humans and domesticated animals. This suggests that on our way to dominating the planet, though we manipulated the genetics of dogs, sheep, cattle and many others to domesticate them, we may have unwittingly done something not too dissimilar to ourselves.