BSCI430 Exam III - Domestication Syndrome Paper

What is Domestication Syndrome?

A suite of behavioral, physiological, and morphological traits consistently found in domesticated animals but not their wild ancestors.

List traits included in Domestication Syndrome.

Increased tameness, depigmentation, floppy ears, smaller jaws and teeth, smaller brains, neoteny, curly tails, and altered reproductive cycles.

What is the Neural Crest Hypothesis?

Domestication traits arise from mild deficits in neural crest cell development, migration, or proliferation.

What are neural crest cells (NCCs)?

Multipotent stem cells originating from the dorsal neural tube that migrate and contribute to many tissues like pigment cells, craniofacial cartilage, and adrenal glands.

How does neural crest hypofunction explain domestication traits?

Reduced or altered NCC development leads to changes in pigmentation, jaw size, ear cartilage, behavior, and adrenal function.

Why is neural crest migration especially important in DS?

Distant body regions (face, limbs, tail) show greater variability, suggesting NCCs failed to reach these areas in sufficient numbers.

What animal model strongly supports the neural crest hypothesis for DS?

The domesticated foxes from Belyaev’s experiment, selectively bred for tameness, which developed DS traits.

What is a neurocristopathy?

A condition caused by defects in neural crest cell development, often used to draw parallels with DS traits.

What is an example of a neurocristopathy relevant to DS?

Waardenburg syndrome—causes pigmentation and craniofacial changes due to neural crest defects.

How could you test the neural crest hypothesis experimentally?

Compare neural crest cell behavior (e.g., number, migration) in wild vs. domesticated animals using GFP-labeled cell tracing.

What would falsify the neural crest hypothesis?

If domesticated animals showed normal NCC development and function compared to wild ancestors.

How could you induce DS-like traits in wild animals experimentally?

By engineering mild NCC deficiencies in wild-type embryos and examining DS phenotypes (e.g., pigmentation, jaw size).