ArticleCell discovery2023
Upf3a but not Upf1 mediates the genetic compensation response induced by leg1 deleterious mutations in an H3K4me3-independent manner.
Article in Cell discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
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- Genomic Exaptation and Regulatory Landscape Shifts as Key Mechanisms Enabling Flatworm Terrestrialization.Genome biology and evolution · 2026Article
- Mechanisms linking cytoplasmic decay of translation-defective mRNA to transcriptional adaptation.Science (New York, N.Y.) · 2026Article
- Integrative and accurate annotations enhance current nonsense-mediated mRNA decay rules.Nucleic acids research · 2025Article
- Cell type- and factor-specific nonsense-mediated RNA decay.Nucleic acids research · 2025Article
- Optimizing gRNA selection for high-penetrance F0 CRISPR screening for interrogating disease gene function.Nucleic acids research · 2025Article
- SelectRepair Knockout: Efficient PTC-Free Gene Knockout Through Selectable Homology-Directed DNA Repair.Methods in molecular biology (Clifton, N.J.) · 2025Article
- RLS-associated MEIS transcription factors control distinct processes in human neural stem cells.Scientific reports · 2024Article
- Prevalence of and gene regulatory constraints on transcriptional adaptation in single cells.Genome biology · 2024Article
- Upf2-Mediated Nonsense-Mediated Degradation Pathway Involved in Genetic Compensation ofInsects · 2024Article
- Prevalence of and gene regulatory constraints on transcriptional adaptation in single cells.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Genetic compensation responses (GCRs) can be induced by deleterious mutations in living organisms in order to maintain genetic robustness. One type of GCRs, homology-dependent GCR (HDGCR), involves transcriptional activation of one or more homologous genes related to the mutated gene. In zebrafish, ~80% of the genetic mutants produced by gene editing technology failed to show obvious phenotypes. The HDGCR has been proposed to be one of the main reasons for this phenomenon. It is triggered by mutant mRNA bearing a premature termination codon and has been suggested to depend on components of both the nonsense mRNA-mediated degradation (NMD) pathway and the complex of proteins associated with Set1 (COMPASS). However, exactly which specific NMD factor is required for HDGCR remains disputed. Here, zebrafish leg1 deleterious mutants are adopted as a model to distinguish the role of the NMD factors Upf1 and Upf3a in HDGCR. Four single mutant lines and three double mutant lines were produced. The RNA-seq data from 71 samples and the ULI-NChIP-seq data from 8 samples were then analyzed to study the HDGCR in leg1 mutants. Our results provide strong evidence that Upf3a, but not Upf1, is essential for the HDGCR induced by nonsense mutations in leg1 genes where H3K4me3 enrichment appears not to be a prerequisite. We also show that Upf3a is responsible for correcting the expression of hundreds of genes that would otherwise be dysregulated in the leg1 deleterious mutant.
Identifiers
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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 Socratic graph.