Altered neural crest development could be the reason mammals change in oddly consistent ways during domestication:
As first noted by Darwin more than 140 years ago, domestic mammals tend to share certain characteristics—a suite of traits called the domestication syndrome.
The syndrome includes increased docility and tameness, coat color changes, reductions in tooth size, changes in craniofacial morphology, alterations in ear and tail form, more frequent and nonseasonal estrus cycles, alterations in hormone levels, changed concentrations of neurotransmitters, prolonged juvenile behavior, and reduced forebrain size.
Wilkins and Wrangham set about listing these mysterious marks of domestication and trying to match them to tissues affected by the neural crest. Within half an hour they decided that neural crest changes could plausibly account for most of the syndrome’s traits.
The neural crest hypothesis builds on observations from the long-running fox domestication experiments started in 1959 in Novosibirsk, Siberia, by Dmitri Belyaev:
After generations of selection purely for tameness, Novosibirsk foxes today show not only a friendly, people-loving disposition reminiscent of dogs, but also seemingly unrelated traits like curly tails, floppier ears and patches of white fur.
One of the many changes seen in the tame foxes was reduced size and function of their adrenal glands, which release stress hormones during the “fight-or-flight” response. This dampened adrenal function may lie at the heart of the behavioral changes observed in domestication syndrome. Wilkins et al. argue that one way to end up with smaller adrenal glands is via mild deficits of the neural crest.
The neural crest is a cell population that pinches off from the edge of the developing neural tube duing early embryogenesis. These cells migrate to many parts of the body and form the precursors of a plethora of tissue types, including pigment cells, parts of the skull, larynx, ears, teeth, sympathetic nervous system, and, of course, parts of the adrenal glands. So subtle changes in neural crest cell numbers, migration, or proliferation would lead to widespread phenotypic effects.
Wilkins et al. argue that their ideas dovetail with certain effects of human neural crest cell disorders, like the patches of depigmented skin and hair seen in Waardenburg syndrome or the jaw, ear and teeth phenotypes of Treacher Collins syndrome.
And even though neural crest cells don’t directly develop into the central nervous system, they could still partly explain why many domestic mammals have smaller forebrains than their wild ancestors. Experiments in chick embryos suggest that signals from neural crest cells play a crucial role in forebrain development. At this stage, not every component of the domestication syndrome can be firmly tied into the hypothesis. For example, the curly tails of dogs, pigs, and domestic foxes don’t have an obvious connection to neural crest deficits. Nonetheless, the authors believe enough links exist to warrant experimental tests of their predictions.