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    Espinosa Medina Lab
    02/27/24 | Haploidy-linked cell proliferation defects limit larval growth in Zebrafish
    Kan Yaguchi , Daiki Saito , Triveni Menon , Akira Matsura , Takeomi Mizutani , Tomoya Kotani , Sreelaja Nair , Ryota Uehara
    bioRxiv. 2024 Feb 27:. doi: 10.1101/2022.05.12.491746

    Haploid larvae in non-mammalian vertebrates are lethal with characteristic organ growth retardation collectively called “haploid syndrome.” In contrast to mammals whose haploid intolerance is attributed to imprinting misregulation, the cellular principle of haploidy-linked defects in non-mammalian vertebrates remains unknown. Here, we investigated cellular defects that disrupt the ontogeny of gynogenetic haploid zebrafish larvae. Unlike diploid control, haploid larvae manifested unscheduled cell death at the organogenesis stage, attributed to haploidy-linked p53 upregulation. Moreover, we found that haploid larvae specifically suffered the gradual aggravation of mitotic spindle monopolarization during 1-3 days post fertilization, causing spindle assembly checkpoint-mediated mitotic arrest throughout the entire body. High-resolution imaging revealed that this mitotic defect accompanied the haploidy-linked centrosome loss occurring concomitantly with the gradual decrease in larval cell size. Either resolution of mitotic arrest or depletion of p53 significantly improved organ growth in haploid larvae. Based on these results, we propose that haploidy-linked mitotic defects and cell death are critical cellular causes that limit the larval growth in the haploid state, potentially placing an evolutionary constraint on allowable ploidy status in the non-mammalian vertebrate life cycle.

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