ArticleNature2019
Genetic compensation triggered by mutant mRNA degradation.
Article in Nature, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 630 papers.
What it found
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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
630 citing papers in PubMed, 1,052 citations in OpenAlex.
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- Article
- High Throughput Characterization of Eukaryotic 2A-Like Peptides Identifies Novel Leucine-Associated Reduction in Protein Abundance.bioRxiv : the preprint server for biology · 2026Article
- Real-time imaging of transcriptional feedback in nonsense-mediated mRNA decay.Science advances · 2026Article
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- isl1a coordinates onset and termination of regeneration of the zebrafish lateral line.NPJ Regenerative medicine · 2026Article
- Elevated phagocytic capacity directs innate spinal cord repair.Cell reports · 2026Article
- Flow-Induced Yap/Taz Signaling Balances Endothelial and Hematopoietic Stem Cell Fates.bioRxiv : the preprint server for biology · 2026Article
570 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 5 institutions in 4 countries.
Funding
Abstract
Genetic robustness, or the ability of an organism to maintain fitness in the presence of harmful mutations, can be achieved via protein feedback loops. Previous work has suggested that organisms may also respond to mutations by transcriptional adaptation, a process by which related gene(s) are upregulated independently of protein feedback loops. However, the prevalence of transcriptional adaptation and its underlying molecular mechanisms are unknown. Here, by analysing several models of transcriptional adaptation in zebrafish and mouse, we uncover a requirement for mutant mRNA degradation. Alleles that fail to transcribe the mutated gene do not exhibit transcriptional adaptation, and these alleles give rise to more severe phenotypes than alleles displaying mutant mRNA decay. Transcriptome analysis in alleles displaying mutant mRNA decay reveals the upregulation of a substantial proportion of the genes that exhibit sequence similarity with the mutated gene's mRNA, suggesting a sequence-dependent mechanism. These findings have implications for our understanding of disease-causing mutations, and will help in the design of mutant alleles with minimal transcriptional adaptation-derived compensation.
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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 OpenQuestion graph.