baz1b loss-of-function in zebrafish produces phenotypic alterations consistent with the domestication syndrome
Jose V. Torres-Pérez,
Sofia Anagianni,
Aleksandra M. Mech,
William Havelange,
Judit García-González,
Scott E. Fraser,
Giorgio Vallortigara,
Caroline H. Brennan
Affiliations
Jose V. Torres-Pérez
School of Biological and Behavioural Sciences, Queen Mary University of London, London E1 4NS, UK; Departament de Biologia Cel·lular, Biologia Funcional i Antropologia física, Fac. de CC. Biològiques, Universitat de València, C/ Dr. Moliner 50, Burjassot, València 46100, Spain; Corresponding author
Sofia Anagianni
School of Biological and Behavioural Sciences, Queen Mary University of London, London E1 4NS, UK
Aleksandra M. Mech
School of Biological and Behavioural Sciences, Queen Mary University of London, London E1 4NS, UK
William Havelange
School of Biological and Behavioural Sciences, Queen Mary University of London, London E1 4NS, UK
Judit García-González
School of Biological and Behavioural Sciences, Queen Mary University of London, London E1 4NS, UK; Department of Genetics and Genomic Sciences, Icahn School of Medicine, Mount Sinai, New York, NY 10029, USA
Scott E. Fraser
Michelson Center for Convergent Bioscience, University of Southern California, Los Angeles, CA, USA
Giorgio Vallortigara
Center for Mind/Brain Sciences, University of Trento, Rovereto, Italy
Caroline H. Brennan
School of Biological and Behavioural Sciences, Queen Mary University of London, London E1 4NS, UK; Corresponding author
Summary: BAZ1B is a ubiquitously expressed nuclear protein with roles in chromatin remodeling, 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 behavioral 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 behavioral phenotypes associated with domestication in addition to craniofacial features. Zebrafish with baz1b LoF show mild underdevelopment at larval stages and distinctive craniofacial features later in life. Mutant zebrafish show reduced anxiety-associated phenotypes and an altered ontogeny of social behaviors. Thus, in zebrafish, developmental deficits in baz1b recapitulate both morphological and behavioral phenotypes associated with the domestication syndrome in other species.
