ArticleScientific reports2023
Poly (A)-specific ribonuclease deficiency impacts oogenesis in zebrafish.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
The trial behind it
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Who cites it
5 citing papers in PubMed.
- Base editors in zebrafish: a new era for functional genomics and disease modeling.Frontiers in genome editing · 2025Review
- Review
- The molecular mechanisms underpinning maternal mRNA dormancy.Biochemical Society transactions · 2024Review
- Assessing the impact of meta-genomic tools on current cutting-edge genome engineering and technology.International journal of biochemistry and molecular biology · 2023Review
- Molecular Interplay of PARN and Telomerase: Tail Modifiers and Disease Implications.Wiley interdisciplinary reviews. RNAReview
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poly (A)-specific ribonuclease (PARN) is the most important 3'-5'exonuclease involved in the process of deadenylation, the removal of poly (A) tails of mRNAs. Although PARN is primarily known for its role in mRNA stability, recent studies suggest several other functions of PARN including a role in telomere biology, non-coding RNA maturation, trimming of miRNAs, ribosome biogenesis and TP53 function. Moreover, PARN expression is de-regulated in many cancers, including solid tumours and hematopoietic malignancies. To better understand the in vivo role of PARN, we used a zebrafish model to study the physiological consequences of Parn loss-of-function. Exon 19 of the gene, which partially codes for the RNA binding domain of the protein, was targeted for CRISPR-Cas9-directed genome editing. Contrary to the expectations, no developmental defects were observed in the zebrafish with a parn nonsense mutation. Intriguingly, the parn null mutants were viable and fertile, but turned out to only develop into males. Histological analysis of the gonads in the mutants and their wild type siblings revealed a defective maturation of gonadal cells in the parn null mutants. The results of this study highlight yet another emerging function of Parn, i.e., its role in oogenesis.
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Registered trials
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