ArticleG3 (Bethesda, Md.)2022
Ankfn1-mutant vestibular defects require loss of both ancestral and derived paralogs for penetrance in zebrafish.
Article in G3 (Bethesda, Md.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- A single-nucleus transcriptomic atlas of human inner ear development.Nature neuroscience · 2026Article
- mWAKE in the Central Amygdala Regulates Fear Learning and Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Rapid Detection ofBiomolecules · 2024Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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.
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Registered trials
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