BAZ1B is an ubiquitously expressed nuclear protein with roles in chromatin remodelling, DNA replication and repair, and transcription. Reduced baz1b expression disrupts neuronal and neural crest development. Variation in the activity of baz1b has been proposed to underly morphological and behavioural aspects of domestication through disruption of neural crest development. Knockdown of baz1b in Xenopus embryos and Baz1b loss of function (LoF) in mice leads to craniofacial defects consistent with this hypothesis. We generated baz1b LoF zebrafish using CRISPR/Cas9 gene editing to test the hypothesis that baz1b regulates behavioural phenotypes associated with domestication in addition to craniofacial features. Zebrafish with baz1b LoF show mild under-development at larval stages and distinctive craniofacial features later in life. Mutant zebrafish show reduced anxiety-associated phenotypes and an altered ontogeny of social behaviours. Thus, in zebrafish, developmental deficits in baz1b recapitulate both morphological and behavioural phenotypes associated with the domestication syndrome in other species.