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High-throughput DNA Extraction and Genotyping of 3dpf Zebrafish Larvae by Fin Clipping
Published on: June 29, 2018
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Haploidy-linked cell proliferation defects limit larval growth in zebrafish
Kan Yaguchi1,2, Daiki Saito1, Triveni Menon3
1Graduate School of Life Science, Hokkaido University, Kita 21, Nishi 11, Kita-Ku , Sapporo 001-0021, Japan.
Open Biology
|October 8, 2024
Summary
Haploid zebrafish larvae exhibit lethal organ growth defects due to cell death and mitotic errors. These findings reveal conserved cellular mechanisms underlying haploid syndrome in vertebrates.
Area of Science:
- Developmental Biology
- Genetics
- Cell Biology
Background:
- Haploid syndrome, characterized by organ growth retardation, is lethal in non-mammalian vertebrates.
- While imprinting is implicated in mammals, the cellular basis of haploid defects in other vertebrates is unclear.
Purpose of the Study:
- To investigate the cellular defects causing haploid syndrome in zebrafish larvae.
- To elucidate the molecular and cellular mechanisms underlying haploid intolerance in non-mammalian vertebrates.
Main Methods:
- Gynogenetic haploid zebrafish model generation.
- High-resolution imaging and live imaging techniques.
- Analysis of cell death, cell cycle progression, and centrosome dynamics.
Main Results:
- Haploid larvae showed increased cell death during organogenesis, linked to p53 upregulation.
- Mitotic spindle monopolarization and subsequent mitotic arrest were observed in haploid larvae.
- Centrosome loss and decreased cell size accompanied mitotic defects in haploid larvae.
- Partial rescue of organ growth was achieved by resolving mitotic arrest or depleting p53.
Conclusions:
- Haploidy-induced mitotic defects and cell death are critical cellular causes of haploid syndrome.
- These findings suggest conserved cellular mechanisms limit larval growth in haploid vertebrates.
- This contributes to an evolutionary constraint on ploidy status in the vertebrate life cycle.

