Dataset Information

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

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.

SUBMITTER: Torres-Perez JV

PROVIDER: S-EPMC9793288 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature

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

Torres-Pérez Jose V JV Anagianni Sofia S Mech Aleksandra M AM Havelange William W García-González Judit J Fraser Scott E SE Vallortigara Giorgio G Brennan Caroline H CH

iScience 20221201 1

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 ...[more]

PMID: 36582821

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Project description:The transformation of wild plants into domesticated crops usually modifies a common set of characters referred to as 'domestication syndrome' traits such as the loss of pod shattering/seed dehiscence, loss of seed dormancy, reduced anti-nutritional compounds and changes in growth habit, phenology, flower and seed colour. Understanding the genetic control of domestication syndrome traits facilitates the efficient transfer of useful traits from wild progenitors into crops through crossing and selection. Domesticated forms of yellow lupin (Lupinus luteus L.) possess many domestication syndrome traits, while their genetic control remains a mystery. This study aimed to reveal the genetic control of yellow lupin domestication traits. This involved phenotypic characterisation of those traits, defining the genomic regions controlling domestication traits on a linkage map and performing a comparative genomic analysis of yellow lupin with its better-understood relatives, narrow-leafed lupin (L. angustifolius L.) and white lupin (L. albus L.). We phenotyped an F9 recombinant inbred line (RIL) population of a wide cross between Wodjil (domesticated) × P28213 (wild). Vernalisation responsiveness, alkaloid content, flower and seed colour in yellow lupin were each found to be controlled by single loci on linkage groups YL-21, YL-06, YL-03 and YL-38, respectively. Aligning the genomes of yellow with narrow-leafed lupin and white lupin revealed well-conserved synteny between these sister species (76% and 71%, respectively). This genomic comparison revealed that one of the key domestication traits, vernalisation-responsive flowering, mapped to a region of conserved synteny with the vernalisation-responsive flowering time Ku locus of narrow-leafed lupin, which has previously been shown to be controlled by an FT homologue. In contrast, the loci controlling alkaloid content were each found at non-syntenic regions among the three species. This provides a first glimpse into the molecular control of flowering time in yellow lupin and demonstrates both the power and the limitation of synteny as a tool for gene discovery in lupins.

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

Publications

<i>baz1b</i> loss-of-function in zebrafish produces phenotypic alterations consistent with the domestication syndrome.

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