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Cited by 830Developmental Biology and Gene RegulationRNA Research and SplicingZebrafish Biomedical Research Applications

The DOI matches its Crossref record; 156 of the 156 references it cites were found in a registry or an index.

Genetic compensation: A phenomenon in search of mechanisms

Open access
El-Brolosy, Mohamed A., Stainier, Didier Y. R.·2017·PLOS Genetics
DOI 10.1371/journal.pgen.1006780PMC PMC5509088
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Abstract

Several recent studies in a number of model systems including zebrafish, Arabidopsis, and mouse have revealed phenotypic differences between knockouts (i.e., mutants) and knockdowns (e.g., antisense-treated animals). These differences have been attributed to a number of reasons including off-target effects of the antisense reagents. An alternative explanation was recently proposed based on a zebrafish study reporting that genetic compensation was observed in egfl7 mutant but not knockdown animals. Dosage compensation was first reported in Drosophila in 1932, and genetic compensation in response to a gene knockout was first reported in yeast in 1969. Since then, genetic compensation has been documented many times in a number of model organisms; however, our understanding of the underlying molecular mechanisms remains limited. In this review, we revisit studies reporting genetic compensation in higher eukaryotes and outline possible molecular mechanisms, which may include both transcriptional and posttranscriptional processes.

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Fig 1 Proposed models of transcriptional adaptation. (A) DNA damage response can induce chromatin reorganization, increasing chromatin accessibility at the compensatory genes’ regulatory regions. (B) Mutations can lead to transcripts that are targeted for degradation through mRNA surveillance pathways. The resulting RNA fragments may trigger the compensatory response. As a secondary effect of the mutated gene’s mRNA degradation, RBPs or miRNAs normally acting on the mutated as well as the compensating genes’ mRNAs become more available to exert their stabilizing effects on the compensating genes’ mRNAs. Abbreviations: miRNAs, microRNAs; RBPs, RNA-binding proteins; TFs, transcription factors.
Fig 1 Proposed models of transcriptional adaptation. (A) DNA damage response can induce chromatin reorganization, increasing chromatin accessibility at the compensatory genes’ regulatory regions. (B) Mutations can lead to transcripts that are targeted for degradation through mRNA surveillance pathways. The resulting RNA fragments may trigger the compensatory response. As a secondary effect of the mutated gene’s mRNA degradation, RBPs or miRNAs normally acting on the mutated as well as the compensating genes’ mRNAs become more available to exert their stabilizing effects on the compensating genes’ mRNAs. Abbreviations: miRNAs, microRNAs; RBPs, RNA-binding proteins; TFs, transcription factors.CC BY · PubMed Central

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Research works printed but not linked: 2

  1. Muller HJ, editor Further studies on the nature and causes of gene mutations. Proceedings of the 6th International Congress of Genetics; 1932.
  2. A Hagelkruys, 2014, A single allele of Hdac2 but not Hdac1 is sufficient for normal mouse brain development in the absence of its paralog, Development (Cambridge, England), 141, 604, 10.1242/dev.100487 · DOI · Paper page

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Metadata

Authors
El-Brolosy, M. A., & Stainier, D. Y. R.
Affiliations
Max Planck Institute for Heart and Lung Research (DE)
Corresponding author
Stainier, Didier Y. R.
ORCID
Venue
PLOS Genetics
Publisher
Public Library of Science (PLoS)
Published
2017-07-13
Volume
13
Issue
7
Pages
e1006780
ISSN
  • 1553-7390 (ISSN-L)
  • 1553-7404
DOI
10.1371/journal.pgen.1006780
PMC
PMC5509088
OpenAlex
W2735720719
Cited by
829
References
156
Citations by year
2026: 60 · 2025: 84 · 2024: 89 · 2023: 91 · 2022: 114 · 2021: 109 · 2020: 120 · 2019: 104 · 2018: 54 · 2017: 4
FWCI
7.22
Type
journal article
Language
en
Open access
Licence
Locations
  • PLoS Genetics (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • MPG.PuRe (Max Planck Society) (submittedVersion)
Funders
  • Deutsche Forschungsgemeinschaft
  • Max-Planck-Gesellschaft
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Zebrafish Biomedical Research Applications
Keywords
genetic compensation, dosage compensation, gene knockout, gene knockdown, off-target effects, EGFL7, transcriptional regulation, post-transcriptional regulation, molecular mechanisms
MeSH terms
Animals, Dosage Compensation, Genetic, Drosophila, Transcription, Genetic, Zebrafish, Arabidopsis, Models, Animal, Zebrafish Proteins, Mutant Proteins, Mice, Gene Knockdown Techniques, Gene Knockout Techniques

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