ArticleProceedings of the National Academy of Sciences of the United States of America2021
Expression attenuation as a mechanism of robustness against gene duplication.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 59 citations in OpenAlex.
- The shape of fitness functions and the distribution of mutational effect sizes jointly limit adaptation by regulatory mutations.Nature ecology & evolution · 2026Article
- Molecular evolution in light of regulatory-coding epistasis.EMBO reports · 2026Review
- Evolutionary causes and consequences of gene duplication.Nature reviews. Genetics · 2026Review
- Protein-protein interactions are a major source of epistasis in genetic interaction networks.Nature communications · 2026Article
- Transcriptomic and proteomic ramifications of segmental amplification inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Multilevel Gene Expression Changes in Lineages Containing Adaptive Copy Number Variants.Molecular biology and evolution · 2025Article
- A compendium of Amplification-Related Gain Of Sensitivity genes in human cancer.Nature communications · 2025Article
- The role of gene copy number variation in antimicrobial resistance in human fungal pathogens.npj antimicrobials and resistance · 2025Review
- How genotype-by-environment interactions on fitness emerge.Nature ecology & evolution · 2024Article
- Article
- Comparative modeling reveals the molecular determinants of aneuploidy fitness cost in a wild yeast model.Cell genomics · 2024Article
- The response to single-gene duplication implicates translation as a key vulnerability in aneuploid yeast.PLoS genetics · 2024Article
- Multilevel gene expression changes in lineages containing adaptive copy number variants.bioRxiv : the preprint server for biology · 2024Article
- Epigenetic diversity of genes with copy number variations among natural populations of the three-spined stickleback.Evolutionary applications · 2024Article
- Comparative modeling reveals the molecular determinants of aneuploidy fitness cost in a wild yeast model.bioRxiv : the preprint server for biology · 2024Article
- Genomic analyses elucidateEcology and evolution · 2024Article
- Compensatory mutations potentiate constructive neutral evolution by gene duplication.bioRxiv : the preprint server for biology · 2024Article
- Expectations of duplicate gene retention under the gene duplicability hypothesis.BMC ecology and evolution · 2023Article
- Parallel Nonfunctionalization of CK1δ/ε Kinase Ohnologs Following a Whole-Genome Duplication Event.Molecular biology and evolution · 2023Article
- Parallel nonfunctionalization of CK1δ/ε kinase ohnologs following a whole-genome duplication event.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Gene duplication is ubiquitous and a major driver of phenotypic diversity across the tree of life, but its immediate consequences are not fully understood. Deleterious effects would decrease the probability of retention of duplicates and prevent their contribution to long-term evolution. One possible detrimental effect of duplication is the perturbation of the stoichiometry of protein complexes. Here, we measured the fitness effects of the duplication of 899 essential genes in the budding yeast using high-resolution competition assays. At least 10% of genes caused a fitness disadvantage when duplicated. Intriguingly, the duplication of most protein complex subunits had small to nondetectable effects on fitness, with few exceptions. We selected four complexes with subunits that had an impact on fitness when duplicated and measured the impact of individual gene duplications on their protein-protein interactions. We found that very few duplications affect both fitness and interactions. Furthermore, large complexes such as the 26S proteasome are protected from gene duplication by attenuation of protein abundance. Regulatory mechanisms that maintain the stoichiometric balance of protein complexes may protect from the immediate effects of gene duplication. Our results show that a better understanding of protein regulation and assembly in complexes is required for the refinement of current models of gene duplication.
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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.