ReviewGenes & diseases2023
The recent advances and future perspectives of genetic compensation studies in the zebrafish model.
Review in Genes & diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 58 citations in OpenAlex.
- FoxO transcription factors coordinate the urea cycle and gluconeogenesis by controllingiScience · 2026Article
- A Framework for Selecting Zebrafish Models of Metabolic Diseases: Modeling Strategies, Phenotypic Validation, Mechanistic Investigation, and Efficacy Evaluation.Biomedicines · 2026Review
- Neurobehavioral Impacts of the Autism Risk Gene, WAC: Studies Involving C. elegans and Mice.Molecular neurobiology · 2026Article
- Actin Isovariant ACT2-Mediated Cellular Auxin Homeostasis Regulates Lateral Root Organogenesis in Arabidopsis thaliana.Cytoskeleton (Hoboken, N.J.) · 2026Article
- Article
- METTL16 in cancer: Roles and regulatory mechanisms.Genes & diseases · 2026Review
- Zebrafish model for studying vascular development and vascular-related disease.Frontiers in cell and developmental biology · 2026Review
- Impact of maternal compensation on developmental phenotypes in a zebrafish model of severe congenital muscular dystrophy.PLoS genetics · 2026Article
- Article
- Potentiation of ryanodine receptor-mediated calcium release by MAPK is responsible for epidermal transformation and carcinogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Integrative and accurate annotations enhance current nonsense-mediated mRNA decay rules.Nucleic acids research · 2025Article
- Morpholino Knockdown in Zebrafish: A Tool to Investigate the Functional Impact of Variants of Unknown Significance in Mitochondrial Diseases.Neuromolecular medicine · 2025Review
- Disruption ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Mutation of Brain Aromatase Impairs Behavior and Neuroplasticity in Adult Zebrafish.Journal of neurochemistry · 2025Article
- Article
- CRISPR/Cas9 Knockout of Shell Matrix Protein 1 in the Slipper-Snail Crepidula atrasolea.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2025Article
- Due-B Is dispensable for early development and genome duplication in vertebrates.bioRxiv : the preprint server for biology · 2025Article
- Monoallelic de novo variants in DDX17 cause a neurodevelopmental disorder.Brain : a journal of neurology · 2025Article
- Article
- Follistatin like-1 (Adipocyte · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic compensation is a remarkable biological concept to explain the genetic robustness in an organism to maintain its fitness and viability if there is a disruption occurred in the genetic variation by mutation. However, the underlying mechanism in genetic compensation remain unsolvable. The initial concept of genetic compensation has been studied in model organisms when there was a discrepancy between knockout-mediated and knockdown-mediated phenotypes. In the zebrafish model, several studies have reported that zebrafish mutants did not exhibit severe phenotype as shown in zebrafish morphants for the same genes. This phenomenon in zebrafish mutants but not morphants is due to the response of genetic compensation. In 2019, two amazing works partially uncovered genetic compensation could be triggered by the upregulation of compensating genes through regulating NMD and/or PTC-bearing mRNA in collaboration with epigenetic machinery in mutant zebrafish. In this review, we would like to update the recent advances and future perspectives of genetic compensation studies, which including the hypothesis of time-dependent involvement and addressing the discrepancy between knockout-mediated and knockdown-mediated to study gene function in the zebrafish model. At last, the study of genetic compensation could be a potential therapeutic strategy to treat human genetic disorder related diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.