PUBLICATION

baz1b loss-of-function in zebrafish produces phenotypic alterations consistent with the domestication syndrome

Authors
Torres-Pérez, J.V., Anagianni, S., Mech, A.M., Havelange, W., García-González, J., Fraser, S.E., Vallortigara, G., Brennan, C.H.
ID
ZDB-PUB-221231-2
Date
2022
Source
iScience   26: 105704105704 (Journal)
Registered Authors
Brennan, Caroline, Fraser, Scott E.
Keywords
Behavioral neuroscience, Molecular physiology
MeSH Terms
none
PubMed
36582821 Full text @ iScience
Abstract
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.
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping