ArticlePLoS genetics2017
mRNA processing in mutant zebrafish lines generated by chemical and CRISPR-mediated mutagenesis produces unexpected transcripts that escape nonsense-mediated decay.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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75 citing papers in PubMed.
- Molecular characterization of Cdh12-SCON conditional knockout mice reveals unexpected splicing changes.Transgenic research · 2026Article
- A Perturb-seq map of a differentiation hub reveals synergistic vulnerabilities in KMT2A-rearranged acute myeloid leukemia.Leukemia · 2026Article
- Zebrafish gon4la mutants recapitulate human GON4L-related growth disorders and reveal novel metabolic organs abnormalities.Scientific reports · 2026Article
- Characterization of CTNND2-related neurodevelopmental disease, phenotype-genotype spectrum and WNT dynamics in early neurogenesis.Research square · 2025Article
- Directly Measuring Atherogenic Lipoprotein Kinetics in Zebrafish With the Photoconvertible LipoTimer Reporter.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Mutation of Brain Aromatase Impairs Behavior and Neuroplasticity in Adult Zebrafish.Journal of neurochemistry · 2025Article
- Generation of NOD SCID mice with near-complete deletions of Il2rg and Prkdc for human cancer and HSC engraftment.Transgenic research · 2025Article
- CRISPR GENome and epigenome engineering improves loss-of-function genetic-screening approaches.Cell reports methods · 2025Article
- Systematic optimization and prediction of cre recombinase for precise genome editing in mice.Genome biology · 2025Article
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- KLF2 maintains lineage fidelity and suppresses CD8 T cell exhaustion during acute LCMV infection.Science (New York, N.Y.) · 2025Article
- Smarce1 fine-tunes cardiomyocyte proliferation in the embryonic zebrafish heart.Frontiers in cell and developmental biology · 2025Article
- Follistatin like-1 (Adipocyte · 2024Article
- Loss ofbioRxiv : the preprint server for biology · 2024Article
- Large-Scale Genome-Wide Optimization and Prediction of the Cre Recombinase System for Precise Genome Manipulation in Mice.Research square · 2024Article
- Large-Scale Genome-Wide Optimization and Prediction of the Cre Recombinase System for Precise Genome Manipulation in Mice.bioRxiv : the preprint server for biology · 2024Article
- CRIMP: a CRISPR/Cas9 insertional mutagenesis protocol and toolkit.Nature communications · 2024Article
- Escaping from CRISPR-Cas-mediated knockout: the facts, mechanisms, and applications.Cellular & molecular biology letters · 2024Review
15 more citing papers are in PubMed but not listed here.
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Abstract
As model organism-based research shifts from forward to reverse genetics approaches, largely due to the ease of genome editing technology, a low frequency of abnormal phenotypes is being observed in lines with mutations predicted to lead to deleterious effects on the encoded protein. In zebrafish, this low frequency is in part explained by compensation by genes of redundant or similar function, often resulting from the additional round of teleost-specific whole genome duplication within vertebrates. Here we offer additional explanations for the low frequency of mutant phenotypes. We analyzed mRNA processing in seven zebrafish lines with mutations expected to disrupt gene function, generated by CRISPR/Cas9 or ENU mutagenesis methods. Five of the seven lines showed evidence of altered mRNA processing: one through a skipped exon that did not lead to a frame shift, one through nonsense-associated splicing that did not lead to a frame shift, and three through the use of cryptic splice sites. These results highlight the need for a methodical analysis of the mRNA produced in mutant lines before making conclusions or embarking on studies that assume loss of function as a result of a given genomic change. Furthermore, recognition of the types of adaptations that can occur may inform the strategies of mutant generation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.