ArticleScientific reports2019
Abnormal development of zebrafish after knockout and knockdown of ribosomal protein L10a.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 22 citations in OpenAlex.
- Analysis of microRNA expression reveals convergent evolution of the molecular control of diapause in annual killifishes.Frontiers in genetics · 2025Article
- Research Progress of Ribosomal Proteins in Reproductive Development.International journal of molecular sciences · 2024Review
- Article
- Identification of three small nucleolar RNAs (snoRNAs) as potential prognostic markers in diffuse large B-cell lymphoma.Cancer medicine · 2023Article
- Postnatal microcephaly and retinal involvement expand the phenotype of RPL10-related disorder.American journal of medical genetics. Part A · 2022Article
- Deficiency of ribosomal proteins reshapes the transcriptional and translational landscape in human cells.Nucleic acids research · 2022Article
- Cell autonomous and non-autonomous consequences of deviations in translation machinery on organism growth and the connecting signalling pathways.Open biology · 2022Review
- Systematic mapping of rRNA 2'-O methylation during frog development and involvement of the methyltransferase Fibrillarin in eye and craniofacial development in Xenopus laevis.PLoS genetics · 2022Article
- Using the Zebrafish as a Genetic Model to Study Erythropoiesis.International journal of molecular sciences · 2021Review
- Role ofInternational journal of molecular sciences · 2020Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, to investigate the secondary function of Rpl10a in zebrafish development, morpholino antisense oligonucleotides (MOs) were used to knock down the zebrafish ribosomal protein L10a (rpl10a). At 25 hpf (hours post-fertilization), embryos injected with the rpl10a MO showed an abnormal morphology, including short bodies, curved tails, and small yolk sac extensions. We observed pigment reductions, edema, larger yolk sacs, smaller eyes and smaller yolk sac extensions at 50 hpf. In addition, reductions in the expression of primordial germ cell (PGC) marker genes (nanos1 and vasa) were observed in rpl10a knockdown embryos. A rescue experiment using a rpl10a mRNA co-injection showed the recovery of the morphology and red blood cell production similar to wild-type. Moreover, the CRISPR-Cas9 system was used to edit the sequence of rpl10a exon 5, resulting in a homozygous 5-bp deletion in the zebrafish genome. The mutant embryos displayed a morphology similar to that of the knockdown animals. Furthermore, the loss of rpl10a function led to reduced expression of gata1, hbae3, and hbbe1 (erythroid synthesis) and increased tp53 expression. Overall, the results suggested that Rpl10a deficiency caused delays in embryonic development, as well as apoptosis and anemia, in zebrafish.
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