Behavioural analysis of loss of function zebrafish supports baz1b as master regulator of domestication

Abstract

Domestication is associated with both morphological and behavioural phenotypic changes that differentiate domesticated species from their wild counterparts. Some of the traits are those purposely targeted by the selection process, whilst others co-occur as a result of selection. The combination of traits is referred to as the domestication syndrome and their shared characteristics has given rise to the neural crest domestication syndrome (NCDS) hypothesis. According to this hypothesis, the phenotypic changes are a consequence of a selection towards animals with mild underdevelopment of the neural crest. A similar mechanism is suggested to affect some species of "self-domesticated" animals, including humans. Recent research supports a role for BAZ1B, one of the haplo-insufficient genes in Williams syndrome (WS), in the evolution of craniofacial features of modern humans. Interestingly, WS recapitulates some of the traits observed in the domestication syndrome, including hypersociability and reduced facial bones. However, the evidence linking BAZ1B to behavioural phenotypes associated with domestication is presumptive. Here, we use zebrafish as a model to test the hypothesis that baz1b loss-of-function leads to both morphological and behavioural phenotypes associated with the domestication syndrome by influencing the development of the neural crest. Our research provides further evidence supporting the NCDS hypothesis and bazlbs role in this process.