PUBLICATION

Ankfn1-mutant vestibular defects require loss of both ancestral and derived paralogs for penetrance in zebrafish

Authors
Ross, K.D., Ren, J., Zhang, R., Chi, N.C., Hamilton, B.A.
ID
ZDB-PUB-220202-29
Date
2021
Source
G3 (Bethesda)   12(3): (Journal)
Registered Authors
Chi, Neil C.
Keywords
Ankfn1, Ankfn1-like, Banderuola, nmf9, wide awake, domain architecture, paralogy, penetrance
MeSH Terms
  • Animals
  • Evolution, Molecular*
  • Gene Duplication
  • Mice
  • Organogenesis
  • Penetrance
  • Phylogeny
  • Zebrafish*/genetics
PubMed
35100349 Full text @ G3 (Bethesda)
Abstract
How and to what degree gene duplication events create regulatory innovation, redundancy, or neofunctionalization remain important questions in animal evolution and comparative genetics. Ankfn1 genes are single copy in most invertebrates, partially duplicated in jawed vertebrates, and only the derived copy retained in most mammals. Null mutations in the single mouse homolog have vestibular and neurological abnormalities. Null mutation of the single Drosophila homolog is typically lethal with severe sensorimotor deficits in rare survivors. The functions and potential redundancy of paralogs in species with two copies are not known. Here, we define a vestibular role for Ankfn1 homologs in zebrafish based on the simultaneous disruption of each locus. Zebrafish with both paralogs disrupted showed vestibular defects and early lethality from swim bladder inflation failure. One intact copy at either locus was sufficient to prevent major phenotypes. Our results show that vertebrate Ankfn1 genes are required for vestibular-related functions, with at least partial redundancy between ancestral and derived paralogs.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping